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Objective To explore the effect and mechanism of Huayu Xiaopi Decoction on gastric mucosal injury in rats with precancerous lesions of gastric cancer (PLGC) based on the interleukin-6 (IL-6) /Janus kinase 2 (JAK2) /signal transduction and transcription activating factor 3 (STAT3) pathway. Methods Totally 10 SD rats were randomly selected as a blank group and the remaining 50 rats were used as a model group, which were replicated using a multifactor comprehensive modeling method. After the PLGC model was successfully constructed, rats were randomly divided into model group, folic acid group (0.002 g·kg-1 ), low-, medium- and high- dose of Huayu Xiaopi Decoction (6.2, 12.4, 24.8 g·kg-1 ) groups, and then the corresponding drug was orally administered once a day for three months. The general condition, the body weight and 3-hour food intake of rats were observed. The pathological changes of gastric tissues in each group of rats were observed using hematoxylin-eosin (HE) staining. Enzyme linked immunosorbent assay (ELISA) was used to detect the expression of serum IL-6, interleukin-1β (IL-1β), and tumor necrosis factor alpha (TNF- α) in each rat group. The expression of B-cell lymphoma/leukemia xL (Bcl-xL) and vascular endothelial growth factor (VEGF) in the gastric tissue of rats in each group was detected by fluorescence immunohistochemistry. Western Blot was used to test the protein expression of IL-6, p-JAK2, p-STAT3, Cyclin D1 and c-Myc in the gastric tissues of rats in each group. Results Compared with the blank group, the body weight and 3-hour food intake of rats in the model group were significantly reduced (P＜0.05), the gastric mucosa became thinner and incomplete. Disordered glandular arrangement and reduced glandular number were found. Goblet cells of intestinal metaplasia in gastric epithelial cells and infiltration of inflammatory cells were visible in partial area. The levels of IL-6, IL-1β and TNF-α in the rat serum were also significantly up-regulated (P＜0.05), and the protein expression of IL-6, p-JAK2, p-STAT3, CyclinD1, c-Myc, Bcl-xL and VEGF in gastric tissue was obviously up-regulated (P＜ 0.05) . Compared with the model group, the body weight and 3-hour food intake of rats in medium- and high- dose of Huayu Xiaopi Decoction groups increased (P＜0.05), the gastric mucosal injury were improved with different degree. Glandular arrangement was in order, intestinal metaplasia of gastric epithelial cells was improved, as well as less inflammatory cells were found. The expression of IL-6, TNF- α and IL-1β in the serum of rats remarkably decreased (P＜0.05), while the protein expression of Bcl-xL, VEGF, IL-6, p-JAK2, p-STAT3, CyclinD1 and c-Myc in gastric tissue obviously down-regulated (P＜0.05) . Conclusion Huayu Xiaopi Decoction can effectively improve pathological damage of gastric mucosa in PLGC rats. Its mechanism maybe related to inhibiting inflammatory reaction, and suppressing cell proliferation by regulating the IL-6/JAK2/STAT3 pathway. [ABSTRACT FROM AUTHOR]

Objective Based on transcriptomics and weighted gene co-expression network analysis (WGCNA), this study aims to explore the mechanism of Jiangzhi Qingshen Capsules mediating the nuclear transcription factor (NF) -κB/ NOD like receptor heat protein domain related protein 3 (NLRP3) /cysteine protease-1 (Caspase-1) signaling axis to improve hyperlipidemia. Method Forty C57BL/6 mice were randomly divided into control group, model group, rosuvastatin group (1.3 mg·kg-1 ), Jiangzhi Qingshen Capsules low- and high- dose groups (0.6 and 2.4 g·kg-1 ), with eight mice in each group. Except the control group was given regular feed, other groups were given high-fat feed to replicate the hyperlipidemia model. The treatment groups were orally administered the corresponding drug once a day for 10 consecutive weeks. The mass of rat liver was taken to calculate the liver index, Lee's index and ratio of liver weight to tibia length. Hematoxylin eosin (HE) staining and oil red O staining were used to observe pathological changes in liver tissue. Serum biochemical indicators including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin (IL) -18 and IL-1β were detected by ELISA. The transcriptome sequencing of liver tissue was performed using Bo'ao Jingdian mouse eukaryotic transcriptome chip V4, then WGCNA of chip expression information and the trait data of blood lipid levels was carried out. The core gene groups (potential targets) of Jiangzhi Qingshen Capsule intervention in hyperlipidemia were obtained, and they were further used to perform protein-protein interaction (PPI) network analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis. Real-time fluorescence quantitative polymerase chain reaction (RTqPCR) was used to detect the mRNA levels of NF- κB, NLRP3, Caspase-1, IL-18, and IL-1β in liver, and immunofluorescence was used to detect the protein expression of NF- κB, NLRP3 and Caspase-1 in liver. Results Compared with model group, Jiangzhi Qingshen Capsules effectively reduced the body weight, liver wet weight, liver index, Lee's index and ratio of liver weight to tibia length (P＜0.05), effectively alleviate inflammatory infiltration and steatosis in liver tissue of hyperlipidemic mice, and significantly reduce lipid deposition area (P＜0.05) . Moreover, Jiangzhi Qingshen Capsules obviously improved serum TC, LDL-C, ALT, AST, IL-18, and IL-1β levels (P＜0.05), effectively down-regulated the protein and mRNA expression of NF-κB, NLRP3 and Caspase-1 in liver tissue (P＜0.05), and decreased the mRNA levels of IL-18 and IL-1β (P＜0.05) . Transcriptomics and WGCNA showed that the regulatory effect of Jiangzhi Qingshen Capsules on blood lipids may be closely related to the inflammatory pathway. Conclusion Jiangzhi Qingshen Capsules can inhibit inflammatory reaction in liver tissue of hyperlipidemic mice by mediating the NF-κB/NLRP3/Caspase-1 signaling axis, thereby improving blood lipid levels. [ABSTRACT FROM AUTHOR]

Context: Diabetic peripheral neuropathy (DPN) results in an enormous burden and reduces the quality of life for patients. Considering there is no specific drug for the management of DPN, traditional Chinese medicine (TCM) has increasingly drawn attention of clinicians and researchers around the world due to its characteristics of multiple targets, active components, and exemplary safety. Objective: To summarize the current status of TCM in the treatment of DPN and provide directions for novel drug development, the clinical effects and potential mechanisms of TCM used in treating DPN were comprehensively reviewed. Methods: Existing evidence on TCM interventions for DPN was screened from databases such as PubMed, the Cochrane Neuromuscular Disease Group Specialized Register (CENTRAL), and the Chinese National Knowledge Infrastructure Database (CNKI). The focus was on summarizing and analyzing representative preclinical and clinical TCM studies published before 2023. Results: This review identified the ameliorative effects of about 22 single herbal extracts, more than 30 herbal compound prescriptions, and four Chinese patent medicines on DPN in preclinical and clinical research. The latest advances in the mechanism highlight that TCM exerts its beneficial effects on DPN by inhibiting inflammation, oxidative stress and apoptosis, endoplasmic reticulum stress and improving mitochondrial function. Conclusions: TCM has shown the power latent capacity in treating DPN. It is proposed that more large-scale and multi-center randomized controlled clinical trials and fundamental experiments should be conducted to further verify these findings. [ABSTRACT FROM AUTHOR]

Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus (DM) and has become the main cause of end-stage renal disease worldwide. In recent years, with the increasing incidence of DM, the pathogenesis of DKD has received increasing attention. The pathogenesis of DKD is diverse and complex. Extracellular vesicles (EVs) contain cell-derived membrane proteins, nucleic acids (such as DNA and RNA) and other important cellular components and are involved in intercellular information and substance transmission. In recent years, an increasing number of studies have confirmed that EVs play an important role in the development of DKD. The purpose of this paper is to explain the potential diagnostic value of EVs in DKD, analyze the mechanism by which EVs participate in intercellular communication, and explore whether EVs may become drug carriers for targeted therapy to provide a reference for promoting the implementation and application of exosome therapy strategies in clinical practice. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of compound Xueshuantong combined with viaminate of oral lichen planus (OLP) complicated with chronic periodontitis (CP). Methods This study collected 305 patients with OLP and CP and randomly divided them into two groups. There were 156 patients in the observation group and 149 patients in the control group. All patients receive systemic treatment for CP. The control group was treated with viaminate capsules, and the observation group was treated with compound Xueshuantong Capsules combined with viaminate capsules. Both groups were treated for 4 weeks. Clinical efficacy, serum inflammatory factors [ matrix metalloproteinase-3 (MMP-3), IFN-gamma (IFN-7), interleukin 6 (IL-6) and IL-35 ], oral mucosal pain Visual Analogue Score (VAS), lesion area of OLP, periodontal condition, and adverse reactions were detected. Results Compared to the control group, the total effective rate in the observation group was higher (P < 0.05 ). After treatment, serum MMP-3 and IL-6 levels, oral mucosal VAS score, lesion area of OLP, gingival index and probing depth all decreased in the two groups (P < 0.05 ). The changes of above indicators were more significant in the observation group (P < 0.05). There was no difference in the incidence of adverse reactions between the two groups (P > 0.05). Conclusion Compound Xueshuantong combined with viaminate can effectively improve the symptoms of OLP complicated with CP, and alleviate inflammatory reactions, with good therapeutic effects. [ABSTRACT FROM AUTHOR]

Purpose: To determine the effect of combining Eustachian tube balloon dilatation with triamcinolone acetonide on inflammatory response and immune function in secretory otitis media patients. Methods: Seventy-six (76) patients diagnosed with acute secretory otitis media in the Ninth People's Hospital Affiliated with Shanghai Jiao Tong University, Shanghai, China were randomly assigned to study group (SG) and control group (CG). Patients in CG received 40 mg triamcinolone acetonide injections in the tympanic membrane weekly for 4 weeks, while SG patients were administered Eustachian tube balloon dilatation in addition to triamcinolone acetonide injection. Pre- and posttreatment assessments in the two evaluated groups included the proportion of T lymphocytes, serum inflammatory molecules and Eustachian Tube Score (ETS). Results: The study group exhibited a significantly higher efficacy (92.1 %) than the control group (68.4 %; p < 0.05). In addition, the study group exhibited higher CD8+, CD4+, CD4+/CD8+ ratio and T cells proportion after treatment (p < 0.05). Furthermore, the concentration of serum inflammatory cytokines (PCT, IL-2, IL-4, TNF-α) in SG was significantly lower than that in CG (p < 0.05). Also, the ETS score in CG was lower (3.53 ± 2.40) compared to SG (5.25 ± 2.02) after treatment (p < 0.05). Conclusion: The combination of triamcinolone acetonide and Eustachian tube balloon dilation demonstrates enhanced efficacy in alleviating symptoms, diminishing inflammatory responses and reestablishing immune balance in the treatment of acute secretory otitis media, underscoring its significant promise. Longer follow-up and larger sample size prospective studies are, however, warranted. [ABSTRACT FROM AUTHOR]

To investigate the possible mechanism of action of Jinqi Qingshu granules (JQQSG) in the treatment of community-acquired pneumonia (CAP) by network pharmacology and molecular docking technology. Methods The TCMSP database and SwissTargetPrediction database were used to obtain and screen the active ingredients and targets of JQQSG, and GeneCards, OMIM, TTD, and DisGeNET databases were used to search for the predicted targets of CAP, and the two targets were mapped and then imported into STRING database to construct a PPI network to screen the key targets, and then the GO and KEGG pathway enrichment were analyzed by the DAVID database, and molecular docking was carried out by the AutoDock Tools software. Results 209 active ingredients and 1041 targets of JQQSG were obtained after screening; 312 targets were co-activated with CAP, and 64 core targets were obtained after PPI network screening. 571 biological processes, 68 cellular components, and 199 molecular functions were analyzed by GO enrichment, and 165 KEGG pathways were analyzed by KEGG pathway enrichment, mainly involved in protein action, apoptosis and MAPK signaling pathway. Molecular docking suggests that the core target and the core components all have good binding ability. Conclusion The mechanism of action of JQQSG in the treatment of CAP may be related to its regulation of Akt, MAPK signaling pathway, improvement of oxidative stress, and other pathways to exert antiinflammatory and antioxidant effects, which could lay the foundation for further in-depth study of its specific mechanism of action. [ABSTRACT FROM AUTHOR]

As a gasotransmitter, the role of hydrogen sulfide (H₂S) in preventing and treating osteoporosis has been confirmed in recent years, and its pathophysiological mechanism is gradually elucidated. H₂S counteracts oxidative stress and inflammatory reactions, promotes angiogenesis, regulates intestinal flora and calcium-phosphorus metabolism, thus enhancing bone formation and inhibiting bone resorption, further preventing and treating various types of osteoporosis, such as postmenopausal osteoporosis and, glucocorticoid, or homocysteine-induced osteoporosis. This article summarizes the existing research to provide new insights for further understanding the pathogenesis and treatment of osteoporosis. [ABSTRACT FROM AUTHOR]

Parkinson's disease is one of the most common neurodegenerative disorders characterized by a multitude of motor and non-motor clinical symptoms resulting from the progressive and long-lasting abnormal loss of nigrostriatal dopaminergic neurons. Currently, the available treatments for patients with Parkinson's disease are limited and exert only symptomatic effects, without adequate signs of delaying or stopping the progression of the disease. Atsttrin constitutes the bioengineered protein which ultrastructure is based on the polypeptide chain frame of the progranulin (PGRN), which exerts anti-inflammatory effects through the inhibition of TNFα. The conducted preclinical studies suggest that the therapeutic implementation of Atsttrin may be potentially effective in the treatment of neurodegenerative diseases that are associated with the occurrence of neuroinflammatory processes. The aim of the proposed study was to investigate the effect of direct bilateral intracerebral administration of Atsttrin using stereotactic methods in the preclinical C57BL/6 mouse model of Parkinson's disease inducted by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication. The analysis of the dose dependency effects of the increasing doses of Atsttrin has covered a number of parameters and markers regarding neurodegenerative processes and inflammatory responses including IL-1α, TNFα, IL-6, TH, and TG2 mRNA expressions. Accordingly, the evaluation of the changes in the neurochemical profile included DA, DOPAC, 3-MT, HVA, NA, MHPG, 5-HT, and 5-HIAA concentration levels. The intracerebral administration of Atsttrin into the striatum effectively attenuated the neuroinflammatory reaction in evaluated neuroanatomical structures. Furthermore, the partial restoration of monoamine content and its metabolic turnover were observed. In this case, taking into account the previously described pharmacokinetic profile and extrapolated bioavailability as well as the stability characteristics of Atsttrin, an attempt was made to describe as precisely as possible the quantitative and qualitative effects of increasing doses of the compound within the brain tissue microenvironment in the presented preclinical model of the disease. Collectively, this findings demonstrated that the intracerebral administration of Atsttrin may represent a potential novel therapeutic method for the treatment of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Peritoneal adhesion (PA) refers to the abnormal adhesion of the peritoneum either with the peritoneum itself or with tissues and organs that is caused by abdominopelvic surgery, abdominal infection or peritoneal inflammation. PA is associated with various clinical complications, such as abdominal pain and distension, intestinal obstruction, gastrointestinal disorders and female infertility, and adversely affects the quality of life of patients. Macrophages are essential for PA formation and can undergo polarization into classically activated macrophages (M1) and alternatively activated macrophages (M2), which are influenced by the peritoneal microenvironment. By releasing proinflammatory cytokines and reactive oxygen species, M1 macrophages promote peritoneal inflammatory reactions and the resultant formation of adhesion. In contrast, M2 macrophages secrete anti‐inflammatory cytokines and growth factors to inhibit PA formation and to promote repair and healing of peritoneal tissues, and thereby play a significant anti‐inflammatory role. This review comprehensively explores the function and mechanism of macrophages and their subtypes in PA formation to gain insight into the prevention and treatment of PA based on the modulation of macrophages. [ABSTRACT FROM AUTHOR]

Objective To investigate the neuroprotective effect and mechanism of salvia polyphenolic acid for injection (SAFI) on cerebral ischemia-reperfusion injury in rats. Methods A total of 100 SD rats were randomly divided into sham surgery group, model group, low, medium and high dose (5, 10, 20 mg·kg-1) salvia polyphenolic acid groups, with 20 rats in each group. After being continuously administrated by intraperitoneal injection of SAFI once daily for three days, the rat model of middle cerebral artery occlusion/reperfusion (MCAO/ R) was established using the thread embolization method at 1 hour after the last administration. The neurological deficit of rats was evaluated by Zea Longa score. The cerebral infarction volume was detected by 2, 3, 5- triphenyltetrazolium chloride (TTC) staining. The levels of serum NADPH oxidase (NOX), 4-hydroxynonanal (4- HNE), 8-hydroxydeoxyguanosine (8-OHdG), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-18 (IL-18), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) were detected by ELISA kits. Hematoxylin-eosin (HE) staining and Nissl staining were used to observe the pathological changes of brain tissue and the morphology of neurons. The apoptosis of neuronal cells in brain tissue was detected by TUNEL. Immunofluorescence staining was used to detect the expression level of glial fibrillary acidic protein (GFAP) in brain tissue. Western Blot was used to detect the protein expression of NLRP3 and Caspasel in brain tissue. Results Compared with the sham surgery group, neurological deficit scores in model group increased remarkably (P<0.01). The cerebral infarction volume increased significantly (P<0.01). Serious pathological damage of brain was observed, and neuronal density decreased significantly (P<0.01). The apoptosis rate of cortical cells increased obviously (P<0.01). The levels of serum NOX, 4-HNE, 8-OHJC, MCP-1, TNF-α, IL-1β, IL-1β, IL-6 and ICAM-1 increased significantly (P<0.05, P<0.01). The protein expression of GFAP, NLRP3 and Caspasel in brain significantly upregulated (P<0.01). Compared with the model group, neurological deficit scores in medium and high dose SAFI groups decreased remarkably (P<0.01). The cerebral infarction volume decreased significantly (P<0.01). Neuronal damage was ameliorated to varying degrees, and neuronal density increased significantly (P<0.05, P<0.01). The apoptosis rate of cortical cells decreased obviously (P<0.01). The levels of serum NOX, 4-HNE, 8-OHJC, MCP-1, TNF-α, IL-1β, IL-18, IL-6 and ICAM-1 decreased significantly (P<0.05, P<0.01). The protein expression of GFAP, NLRP3 and Caspasel in brain significantly downregulated (P<0.01). Conclusion SAFI has a protective effect on MCAO/R rats, which can significantly reduce oxidative stress and inflammatory responses, thereby reducing pathological damage and apoptosis of brain tissue. Its mechanism may be related to the inhibition of NLRP3/Caspase-1 signaling pathway and astrocyte activation. [ABSTRACT FROM AUTHOR]

The handheld nonthermal plasma (HNP) treatment may alter the surface properties, bone metabolism, and inflammatory reactions of polyaryletherketone (PAEK) dental implant materials. This study tested whether the HNP treatment might increase the biocompatibility, surface hydrophilicity, surface free energies (SFEs), and the cell adhesion and mineralization capability of PAEK materials. Disk-shaped samples of titanium (Ti), zirconia (Zr), polyetheretherketone (PEEK [PE]), and polyetherketoneketone (PEKK [PK]) were subjected to HNP treatment and termed as TiPL, ZrPL, PEPL, and PKPL, respectively. Water-surface reactions were examined using a goniometer. MG-63 cells were cultured on all samples to assess the cell viability, cytotoxicity, cell attachment, and mineralization characteristics. The expression of pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) and key mineralization markers (alkaline phosphatase [ALKP], osteopontin [OPN], and dentin matrix protein 1 [DMP1]) was measured using enzyme-linked immunosorbent assay kits. The HNP-treated samples exhibited significantly enhanced surface hydrophilicities and SFEs compared to the untreated samples. The cell viability remained high across all samples, indicating no cytotoxic effects. The HNP treatment significantly enhanced MG-63 cell adherence and proliferation. Elevated levels of ALKP and OPN were observed for the plasma-treated PEPL and PKPL specimens, while DMP1 levels increased significantly only in the PKPL specimen. Pro-inflammatory cytokine levels were low across all samples, suggesting no inflammatory response. The HNP-treated PAEKs have enhanced the surface hydrophilicity and SFEs as well as superior cell adhesion and mineralization capability, and thus may be good clinical dental implant materials. [ABSTRACT FROM AUTHOR]

Context Diabetic peripheral neuropathy (DPN) results in an enormous burden and reduces the quality of life for patients. Considering there is no specific drug for the management of DPN, traditional Chinese medicine (TCM) has increasingly drawn attention of clinicians and researchers around the world due to its characteristics of multiple targets, active components, and exemplary safety.Objective To summarize the current status of TCM in the treatment of DPN and provide directions for novel drug development, the clinical effects and potential mechanisms of TCM used in treating DPN were comprehensively reviewed.Methods Existing evidence on TCM interventions for DPN was screened from databases such as PubMed, the Cochrane Neuromuscular Disease Group Specialized Register (CENTRAL), and the Chinese National Knowledge Infrastructure Database (CNKI). The focus was on summarizing and analyzing representative preclinical and clinical TCM studies published before 2023.Results This review identified the ameliorative effects of about 22 single herbal extracts, more than 30 herbal compound prescriptions, and four Chinese patent medicines on DPN in preclinical and clinical research. The latest advances in the mechanism highlight that TCM exerts its beneficial effects on DPN by inhibiting inflammation, oxidative stress and apoptosis, endoplasmic reticulum stress and improving mitochondrial function.Conclusions TCM has shown the power latent capacity in treating DPN. It is proposed that more large-scale and multi-center randomized controlled clinical trials and fundamental experiments should be conducted to further verify these findings.

Background/purpose: The handheld nonthermal plasma (HNP) treatment may alter the surface properties, bone metabolism, and inflammatory reactions of polyaryletherketone (PAEK) dental implant materials. This study tested whether the HNP treatment might increase the biocompatibility, surface hydrophilicity, surface free energies (SFEs), and the cell adhesion and mineralization capability of PAEK materials. Materials and methods: Disk-shaped samples of titanium (Ti), zirconia (Zr), polyetheretherketone (PEEK [PE]), and polyetherketoneketone (PEKK [PK]) were subjected to HNP treatment and termed as TiPL, ZrPL, PEPL, and PKPL, respectively. Water-surface reactions were examined using a goniometer. MG-63 cells were cultured on all samples to assess the cell viability, cytotoxicity, cell attachment, and mineralization characteristics. The expression of pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) and key mineralization markers (alkaline phosphatase [ALKP], osteopontin [OPN], and dentin matrix protein 1 [DMP1]) was measured using enzyme-linked immunosorbent assay kits. Results: The HNP-treated samples exhibited significantly enhanced surface hydrophilicities and SFEs compared to the untreated samples. The cell viability remained high across all samples, indicating no cytotoxic effects. The HNP treatment significantly enhanced MG-63 cell adherence and proliferation. Elevated levels of ALKP and OPN were observed for the plasma-treated PEPL and PKPL specimens, while DMP1 levels increased significantly only in the PKPL specimen. Pro-inflammatory cytokine levels were low across all samples, suggesting no inflammatory response. Conclusion: The HNP-treated PAEKs have enhanced the surface hydrophilicity and SFEs as well as superior cell adhesion and mineralization capability, and thus may be good clinical dental implant materials.

Background The incidence of acute ischemic stroke (AIS) remains high, and a timely restoration of cerebral blood flow is crucial for its prognosis. There are less therapeutic approaches to promote recovery of cerebral blood flow in AIS patients treated beyond a limited time window. The analysis of remote ischemic postconditioning (RIPostC) on the efficacy, complications and prognosis of AIS patients beyond the time window is of great significance. Objective To investigate the role of RIPostC on the prognosis of AIS beyond time window, thus providing a safe and effective cerebral blood flow restoration way for AIS beyond time window. Methods It was a randomized, parallel group, placebo-controlled trial involving AIS patients beyond time window (onset time > 6 h) of thrombolysis who were hospitalized in the Department of Neurology, Beijing Aerospace General Hospital from September 2, 2021 to August 31, 2022. They were randomly assigned into the control group and experimental group, and treated and followed up for 90 days. General treatment and conventional treatment of cerebrovascular disease were performed in both groups. RIPostC and simulated RIPostC were respectively given 28 times within 14 days in the experimental group and control group, respectively. Before the intervention, and 30 days and 90 days after the intervention, neurological function was assessed using the modified Rankin Scale (mRS) and the National Institutes of Health Stroke Scale (NIHSS). Cognitive function was assessed by the Mini-mental Status Examination (MMSE) and Montreal Cognitive Assessment (MoCA). Daily living ability was assessed by the Instrumental Activity of Daily Living (IADL). Mental status was assessed by the Self-rating Anxiety Scale (SAS) and Self-rating Depression Scale (SDS). Cerebral blood flow velocity was assessed by the transcranial Doppler ultrasound (TCD). Inflammatory response was assessed by measuring interleukin 6 (IL-6) levels. Results Ninety-nine out of 122 AIS patients finally completed the trial and follow-up, including 49 patients in the experimental group and 50 in the control group. There were no significant differences in gender, age, underlying diseases (hypertension, diabetes, coronary heart disease) and baseline NIHSS scores between the two groups (P>0.05). Repeated measures analysis of variance showed that there was an interaction between time and group on MMSE, MoCA, mRS, NIHSS, cerebral blood flow velocity, and IL-6 (P0.05). The incidence of skin ecchymosis [4.00% (2/50) vs. 12.24% (6/49) ] and the overall incidence of adverse events [12.00% (6/50) vs. 34.69% (17/49) ] in the control group were significantly lower than those of the experimental group (P

Objective To analyze the relationship between inflammatory reaction and the short-term readmission of hospitalized patients with chronic obstructive pulmonary disease （COPD） complicated with respiratory failure. Methods Ninety-one hospitalized patients with COPD complicated with respiratory failure were included in this prospective cohort study. They were divided into the occurrence group （n =17） and the non-occurrence group （n =74） according to the occurrence of complications during hospitalization. They were also divided into the readmission group （n =18） and the non-readmission group （n =73） according to the 30-d readmission situation. Another 91 patients with COPD alone were assigned into the control group. The pre-treatment inflammation indicators （white blood cell （WBC）， C-reactive protein （CRP）， tumor necrosis factor-α （TNF-α）） were compared between patients with COPD alone and COPD complicated with respiratory failure and different prognosis. The risk factors of 30-d readmission of COPD complicated with respiratory failure were identified by multivariate binary Logistic regression analysis. The receiver operating characteristic （ROC） curve was delineated to analyze the diagnostic values of these risk factors for the short-term readmission of COPD patients complicated with respiratory failure. Results After treatment， the levels of WBC， CRP， and TNF-α in COPD patients with respiratory failure and simple COPD were significantly lower than those before treatment （all P <0.05）. The levels of WBC， CRP and TNF-α in patients with COPD complicated with respiratory failure before treatment were significantly higher than those in patients with COPD alone （all P <0.05）. The levels of WBC， CRP and TNF-α in COPD patients complicated with type Ⅱ respiratory failure before treatment were significantly higher than those in patients complicated with type Ⅰ respiratory failure （all P <0.05）. The levels of CRP and TNF-α in the occurrence group before treatment were significantly higher than those in the non-occurrence group （both P <0.05）. The levels of CRP and TNF-α in the readmission group before treatment were significantly higher than those in the non-readmission group （both P <0.05）. Multivariate binary logistic regression analysis showed that there was no significant correlation between CRP and TNF-α levels and the 30-d readmission of COPD patients after adjusting for confounding factors （both P >0.05）. However， regardless of the adjustment for confounding factors， CRP and TNF-α levels were significant factors affecting the 30-d readmission of COPD patients with respiratory failure （both P <0.05）. The area under the ROC curve （AUC） of CRP， TNF-α and two combined before treatment for predicting 30-d readmission of COPD patients complicated with respiratory failure all exceeded 0.70， which had certain predictive value. Conclusions CRP and TNF-α yield high efficiency in predicting the short-term readmission of COPD patients complicated with respiratory failure. Treatment plans can be formulated according to CRP and TNF-α levels to reduce the risk of readmission.

Objective: To investigate the effect and mechanism of Hippophae rhamnoides flavone (HRF) on polycystic ovarian syndrome (PCOS) in rats, and to provide new ideas for the prevention and treatment of PCOS. Methods: A PCOS rat model was duplicated by giving rats a high-fat diet combined with the intragastric administration of letrozole, and the model rats were randomly divided into model group, low-dose HRF group (200 mg/kg HRF), high-dose HRF group (400 mg/kg HRF) and metformin group (100 mg/kg). Changes in the related indicators were detected on the 21 d after the rats were administered with the different agents by gavage. Results: Compared with that in the model group, the ovarian index, the percentage of interestrus temporal image, the fasting blood glucose (FBG) level, the fasting insulin (FINS) content, the insulin resistance index (HOMA-IR), the activities of serum luteinizing hormone (LH) and testosterone (T), the levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and C reactive protein (CRP) of rats in low- and high-dose HRF groups were respectively decreased significantly (P

Vernal keratoconjunctivitis is an allergic ocular surface disease mostly present with recurrent chronic inflammation, which usually affects children and adolescents and possibly results in corneal complications such as keratoconus. Keratoconus is a corneal disease characterized by a local cone-like corneal deformation. Previous studies have respectively put forward pathological mechanisms of vernal keratoconjunctivitis and keratoconus and the progressive risk factors, among which we find there's mutual mechanisms as well as cytokines' expression, including type I and IV hypersensitivity, inflammatory reaction, enzymatic changes, oxidative stress and mechanical injury. This review aims at summarizing the possible intrinsic mechanisms and cytokines exacerbating vernal keratoconjunctivitis patients corneas to keratoconus, so as to provide reference for the prevention and management in keratoconus caused by vernal keratoconjunctivitis.

Cell volume as a characteristic of changes in response to external environmental cues has been shown to control the fate of stem cells. However, its influence on macrophage behavior and macrophage-mediated inflammatory responses have rarely been explored. Herein, through mediating the volume of macrophages by adding polyethylene glycol (PEG), we demonstrated the feasibility of fine-tuning cell volume to regulate macrophage polarization towards anti-inflammatory phenotypes, thereby enabling to reverse macrophage-mediated inflammation response. Specifically, lower the volume of primary macrophages can induce both resting macrophages (M0) and stimulated pro-inflammatory macrophages (M1) to up-regulate the expression of anti-inflammatory factors and down-regulate pro-inflammatory factors. Further mechanistic investigation revealed that macrophage polarization resulting from changing cell volume might be mediated by JAK/STAT signaling pathway evidenced by the transcription sequencing analysis. We further propose to apply this strategy for the treatment of arthritis via direct introduction of PEG into the joint cavity to modulate synovial macrophage-related inflammation. Our preliminary results verified the credibility and effectiveness of this treatment evidenced by the significant inhibition of cartilage destruction and synovitis at early stage. In general, our results suggest that cell volume can be a biophysical regulatory factor to control macrophage polarization and potentially medicate inflammatory response, thereby providing a potential facile and effective therapy for modulating macrophage mediated inflammatory responses. Cell volume has recently been recognized as a significantly important biophysical signal in regulating cellular functionalities and even steering cell fate. Herein, through mediating the volume of macrophages by adding polyethylene glycol (PEG), we demonstrated the feasibility of fine-tuning cell volume to induce M1 pro-inflammatory macrophages to polarize towards anti-inflammatory M2 phenotype, and this immunomodulatory effect may be mediated by the JAK/STAT signaling pathway. We also proposed the feasible applications of this PEG-induced volume regulation approach towards the treatment of osteoarthritis (OA), wherein our preliminary results implied an effective alleviation of early synovitis. Our study on macrophage polarization mediated by cell volume may open up new pathways for immune regulation through microenvironmental biophysical clues. [Display omitted] [ABSTRACT FROM AUTHOR]

BACKGROUND: Mesenchymal stem cells are used in flap ischemia-reperfusion injury due to their antioxidant and inflammatory inhibition, and angiogenesis induction. OBJECTIVE: To review the mechanism and latest treatment progress of mesenchymal stem cells in the treatment of flap ischemia-reperfusion injury, and to provide a basis for further theoretical research and clinical rational application. METHODS: We searched the relevant articles indexed in CNKI, WanFang and PubMed databases. Chinese and English search terms were “mesenchymal stem cells; flap ischemia reperfusion injury; conditioned medium; exosomes; oxidative stress; inflammatory reactions; angiogenesis”. Relevant literature since 2010 was searched, and 74 articles were finally included after excluding the literature that had little to do with the topic of the article, poor quality and outdated content. RESULTS AND CONCLUSION: (1) Mesenchymal stem cells play significant roles in antioxidation, inhibition of inflammation and induction of angiogenesis and have great potential in the treatment of flap ischemia-reperfusion injury. (2) However, the defects of mesenchymal stem cells themselves and the decline of therapeutic effect in recent years have put the development and application of mesenchymal stem cells into a bottleneck period, and the research on the plasticity of mesenchymal stem cells conditioned medium and its exosomes and mesenchymal stem cells came into being, and the therapeutic effect was significantly better than the use of mesenchymal stem cells alone. (3) Therefore, a more comprehensive understanding of the mechanism of action and the latest treatment progress of mesenchymal stem cells in the treatment of flap ischemia-reperfusion injury is of great significance for the research of mesenchymal stem cells and the treatment of flap ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

Objective: To explore mechanism of Fasudil reducing Aβ1-42 induced BV2 cell injury based on NLRP3 inflamma‑ some. Methods: BV2 cells were divided into: normal control group, Aβ stimulation group, Aβ +Fasudil intervention group, Aβ + MCC950 (NLRP3 inhibitor) intervention group. Cell morphology was observed under microscope. Cell activity was determined of by CCK8. NO release was measured by Griess. NLRP3, caspase 1 and IL-18 expressions were detected by immunofluorescence staining. NLRP3, ASC, caspase 1, IL-1β and IL-18 expressions were detected by Western blot. Results: Compared with normal control group, BV2 cells in Aβ stimulation group were activated and showed amoeba-like shape, cell activity was decreased, NO production was increased, NLRP3, ASC, caspase 1, IL-1β and IL-18 expressions were increased. Fasudil intervention and MCC950 intervention inhibited cell injury induced by Aβ1-42 in which BV2 cell morphology tended to be normal, cell activity was increased, while produc‑ tion of NO was reduced, and NLRP3, ASC, caspase 1, IL-1β and IL-18 expressions were down-regulated, there was no significant difference between Fasudil intervention group and MCC950 intervention group. Conclusion: Fasudil may alleviate Aβ1-42 induced BV2 cell injury and inflammatory reaction by inhibiting NLRP3 inflammasome activation. [ABSTRACT FROM AUTHOR]

Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Clinical Nursing in Practice is the property of Journal of Clinical Nursing in Practice (Editorial Board, Shanghai Jiao Tong University Press) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the effect and mechanism of Hippophae rhamnoides flavone (HRF) on polycystic ovarian syndrome (PCOS) in rats, and to provide new ideas for the prevention and treatment of PCOS. Methods: A PCOS rat model was duplicated by giving rats a high-fat diet combined with the intragastric administration of letrozole, and the model rats were randomly divided into model group, low-dose HRF group (200 mg/kg HRF), high-dose HRF group (400 mg/kg HRF) and metformin group (100 mg/kg). Changes in the related indicators were detected on the 21 d after the rats were administered with the different agents by gavage. Results: Compared with that in the model group, the ovarian index, the percentage of interestrus temporal image, the fasting blood glucose (FBG) level, the fasting insulin (FINS) content, the insulin resistance index (HOMA-IR), the activities of serum luteinizing hormone (LH) and testosterone (T), the levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and C reactive protein (CRP) of rats in low- and high-dose HRF groups were respectively decreased significantly (P<0.05, P<0.01), while the activity of follicle stimulating hormone FSH) was significantly increased (P<0.01). The histopathological morphology of ovarian tissue of rats treated with the low and high doses of HRF was improved, and the expression levels of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factors-κBp65 (NF-κ Bp65) mRNAs as well as TLR4, MyD88 and p-NF-κBp65 proteins were significantly decreased (P<0.05, P<0.01). Conclusion: HRF could improve the symptoms of PCOS, alleviate the insulin resistance, regulate the level of sex hormones and repair the pathological changes in the ovarian tissue of rats with PCOS, and its mechanism may be related to its inhibition on the inflammatory response mediated by the TLR4/NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

BACKGROUND: Oleic acid can regulate inflammation and immune responses, and has the potential to repair skin wounds. Oleic acid has a short retention time at the lesion. It is prone to self oxidation and deterioration in the air, and suitable drug carriers are needed to fully exert the therapeutic effect of oleic acid. OBJECTIVE: To investigate the efficacy of oleic acid-liposome gel in the treatment of chronic burn wounds. METHODS: Oleic acid liposome solution was prepared by thin film dispersion method, and then dissolved in Poloxamer gel matrix to prepare oleic acidliposome gel. (1) In vitro experiment: Oleic acid-liposome gel solution was prepared by adding different volumes of oleic acid-liposome gel into cell medium (volume ratio: 1:3, 1:9, 1:27, respectively). Alma-blue reagent was used to detect the effects of different concentrations of oleic acid-liposome gel on the proliferation of human keratinocytes and human fibroblasts. Crystal violet staining was used to observe cell morphology. (2) In vivo experiment: The animal model of chronic burn wounds was established by using full-thickness burn of SD rat back skin combined with local subcutaneous injection of epirubicin. The 30 successfully modeled rats were randomly divided into five groups with six rats in each group. The wounds of oleic acid liposome gel group, oleic acid group, liposome gel group, positive control group and negative control group were applied with gauze of oleic acid liposome gel, oleic acid, liposome gel, recombinant human epidermal growth factor gel and normal saline. The dressing was changed once every other day. A total of 16 doses were administered. The wound healing was observed. RESULTS AND CONCLUSION: (1) In vitro experiments: Alma-blue reagent detection and crystal violet staining showed that oleic acid liposome gel solution with volume ratio of 1:9 could promote the proliferation of human keratinocytes and human fibroblasts. (2) In vivo experiment: The wound healing time of the oleic acid liposome gel group was shorter than that of the other four groups (P < 0.01), and the wound healing rate at 4, 8, 12, 16, and 20 days was higher than that of the other four groups (P < 0.01). After administration, hematoxylin-eosin staining showed epithelialization and healing of wounds in all five groups, and the epidermal thickness of oleic acid liposome gel group was the closest to normal skin and better than the other four groups. Immunohistochemical staining showed that the expressions of cytokeratin 10, tumor protein 63, α-smooth muscle actin, collagen I, tumor necrosis factor α, interleukin 6, malonaldehyde, and superoxide dismutase in oleic acid liposome gel group were closest to those in normal skin, and superior to those in other four groups. On days 12 and 32 of administration, the expressions of tumor necrosis factor α, interleukin 6, malondialdehyde, and superoxide dismutase in wound homogenate supernatant in oleic acid liposome gel group were closest to those in normal skin, and superior to those in other four groups. (3) The results showed that oleic acid liposome gel could promote the proliferation of keratinocytes and fibroblasts, reduce inflammation and oxidative stress injury, and promote the healing of chronic burn wounds. [ABSTRACT FROM AUTHOR]

Objective To analyze the relationship between inflammatory reaction and the short-term readmission of hospitalized patients with chronic obstructive pulmonary disease (COPD) complicated with respiratory failure. Methods Ninety-one hospitalized patients with COPD complicated with respiratory failure were included in this prospective cohort study. They were divided into the occurrence group n = 17) and the non-occurrence group (n = 74)according to the occurrence of complications during hospitalization. They were also divided into the readmission group (n = 18)and the non-readmission group ( n = 73 ) according to the 30-d readmission situation. Another 91 patients with COPD alone were assigned into the control group. The pre-treatment inflammation indicators (white blood cell (WBC), C-reactive protein (CRP), tumor necrosis factor-a (TNF-a)) were compared between patients with COPD alone and COPD complicated with respiratory failure and different prognosis. The risk factors of 30-d readmission of COPD complicated with respiratory failure were identified by multivariate binary Logistic regression analysis. The receiver operating characteristic (ROC) curve was delineated to analyze the diagnostic values of these risk factors for the short-term readmission of COPD patients complicated with respiratory failure. Results After treatment, the levels of WBC, CRP, and TNF-a in COPD patients with respiratory failure and simple COPD were significantly lower than those before treatment (all P < 0.05 ). The levels of WBC, CRP and TNF-a in patients with COPD complicated with respiratory failure before treatment were significantly higher than those in patients with COPD alone (all P < 0.05 ). The levels of WBC, CRP and TNF-a in COPD patients complicated with type II respiratory failure before treatment were significantly higher than those in patients complicated with type I respiratory failure (all P < 0.05 ). The levels of CRP and TNF-a in the occurrence group before treatment were significantly higher than those in the non-occurrence group (both P < 0.05 ). The levels of CRP and TNF-a in the readmission group before treatment were significantly higher than those in the non-readmission group (both P < 0.05 ). Multivariate binary logistic regression analysis showed that there was no significant correlation between CRP and TNF-a levels and the 30-d readmission of COPD patients after adjusting for confounding factors (both P > 0.05 ). However, regardless of the adjustment for confounding factors, CRP and TNF-a levels were significant factors affecting the 30-d readmission of COPD patients with respiratory failure (both P < 0.05 ). The area under the ROC curve (AUC)of CRP, TNF-a and two combined before treatment for predicting 30-d readmission of COPD patients complicated with respiratory failure all exceeded 0.70, which had certain predictive value. Conclusions CRP and TNF-a yield high efficiency in predicting the short-term readmission of COPD patients complicated with respiratory failure. Treatment plans can be formulated according to CRP and TNF-a levels to reduce the risk of readmission. [ABSTRACT FROM AUTHOR]

Pyruvate kinase M2 (PKM2) is a key rate-limiting enzyme in glycolysis. It is well known that PKM2 plays a vital role in the proliferation of tumor cells. However, PKM2 can also exert its biological functions by mediating multiple signaling pathways in neurological diseases, such as Alzheimer's disease (AD), cognitive dysfunction, ischemic stroke, post-stroke depression, cerebral small-vessel disease, hypoxic-ischemic encephalopathy, traumatic brain injury, spinal cord injury, Parkinson's disease (PD), epilepsy, neuropathic pain, and autoimmune diseases. In these diseases, PKM2 can exert various biological functions, including regulation of glycolysis, inflammatory responses, apoptosis, proliferation of cells, oxidative stress, mitochondrial dysfunction, or pathological autoimmune responses. Moreover, the complexity of PKM2's biological characteristics determines the diversity of its biological functions. However, the role of PKM2 is not entirely the same in different diseases or cells, which is related to its oligomerization, subcellular localization, and post-translational modifications. This article will focus on the biological characteristics of PKM2, the regulation of PKM2 expression, and the biological role of PKM2 in neurological diseases. With this review, we hope to have a better understanding of the molecular mechanisms of PKM2, which may help researchers develop therapeutic strategies in clinic. [ABSTRACT FROM AUTHOR]

Chronic sinusitis is a common inflammatory disease of the nasal and sinus mucosa, leading to symptoms such as nasal congestion, runny nose, decreased sense of smell, and headache. It often recurs and seriously affects the quality of life of patients. However, its pathological and physiological mechanisms are not fully understood. In recent years, the role of potassium ion channels in the regulation of mucosal barrier function and inflammatory cell function has received increasing attention. In chronic sinusitis, there are often changes in the expression and function of potassium channels, leading to mucosal damage and a stronger inflammatory response. However, the related research is still in its early stages. This article will review the role of the potassium channel in the pathological and physiological changes of chronic sinusitis. The studies revealed that BK/TREK-1 potassium channel play a protective role in the nasal mucosal function through p38-MAPK pathway, and KCa3.1/Kv1.3 enhance the inflammatory response of Chronic rhinosinusitis by regulating immune cell function, intracellular Ca2+ signaling and ERK/MAPK/NF-κB pathway. Because ion channels are surface proteins of cell membranes, they are easier to intervene with drugs, and the results of these studies may provide new effective targets for the prevention and treatment of chronic sinusitis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of NEAT1 targeted regulation of miR‐125/ADAM9 mediated NF‐κB pathway in inflammatory response in rosacea. Method: HaCaT cell rosacea phenotype was induced by LL37. The connection targeted by NEAT1 and miR‐125a‐5p was confirmed by Double‐Luciferase report analysis. qPCR was employed to assess the levels of expression for NEAT1, miR‐125a‐5p, and ADAM9 genes. The levels of expression for ADAM9/TLR2/NF‐κB P65 pathway proteins in each batch of cells were determined by Western blotting. The levels of expression for inflammatory factors, including TNF‐α, IL‐1β, IL‐6, and IL‐18, were measured through ELISA experimentation. Results: LL37 could successfully induce HaCaT cells to exhibit rosacea phenotype. The luciferase report experiment confirmed that NEAT1 could target and bind miR‐125a‐5p and inhibit its expression. ADAM9 exhibited increased expression in LL37‐induced HaCaT cells, showing a positive association with NEAT1 expression and inverse relationship with miR‐125a‐5p activation. LL37 treatment promoted the expression of ADAM9/TLR2/NF‐κB P65 pathway proteins. Silencing ADAM9 can inhibit the inflammatory signaling pathway and reduce the level of TNF‐α, IL‐1β, IL‐6, and IL‐18 in HaCaT cells. Conclusion: NEAT1 can suppress the production of miR‐125a‐5p and activate the TLR2/NF‐κB inflammatory pathway mediated by ADAM9, thereby promoting the inflammatory response in rosacea. [ABSTRACT FROM AUTHOR]

Copyright of Traditional Chinese Drug Research & Clinical Pharmacology is the property of Traditional Chinese Drug Research & Clinical Pharmacology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Diabetic kidney disease (DKD) is a serious complication of diabetes mellitus (DM) and has become the main cause of end-stage renal disease worldwide. In recent years, with the increasing incidence of DM, the pathogenesis of DKD has received increasing attention. The pathogenesis of DKD is diverse and complex. Extracellular vesicles (EVs) contain cell-derived membrane proteins, nucleic acids (such as DNA and RNA) and other important cellular components and are involved in intercellular information and substance transmission. In recent years, an increasing number of studies have confirmed that EVs play an important role in the development of DKD. The purpose of this paper is to explain the potential diagnostic value of EVs in DKD, analyze the mechanism by which EVs participate in intercellular communication, and explore whether EVs may become drug carriers for targeted therapy to provide a reference for promoting the implementation and application of exosome therapy strategies in clinical practice.

Excess weight gain is a growing concern worldwide, fueled by increased consumption of calorie-dense foods and more sedentary lifestyles. Obesity in China is also becoming increasingly problematic, developing into a major public health concern. Obesity not only increases the risk of associated disease but also imposes a burden on health care systems, and it is thus imperative that an effective intervention approach be identified. Recent studies have demonstrated that the polyphenol-rich Mediterranean diet has considerable potential in this regard. Polyphenols can inhibit the production of adipocytes and reduce adverse reactions, such as inflammation, insulin resistance, and gut microflora imbalance. In this review, we examine four polyphenols (curcumin, ellagic acid, ferulic acid, and quercetin) in terms of their potential as interventions targeting obesity. The mechanisms that help promote adipocyte browning, increase thermogenic factors, increase thermogenesis, and regulate adipocyte differentiation are summarized, and key signaling pathways, including PPARγ, C/EBP-, and others, are reviewed.

Ischemic stroke is a common acute cerebrovascular disease in clinical practice， which poses a severe threat to human health. In recent years， with deepening understanding of ischemic stroke， significant progress has been made in the diagnosis and treatment. However， current treatments for ischemic stroke are partially limited due to extremely complex pathological mechanisms. Studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of ischemic stroke. Therefore， modulation of mitochondrial function through mitochondrial dynamics is essential to ameliorate the damage of cerebral ischemic neuronal cells. In this article， the molecular mechanism of mitochondrial dynamics and its role in ischemic stroke were reviewed， aiming to provide useful reference for the treatment of ischemic stroke.

Background. In recent years, a wider range of bakery products with a lower glycaemic response can be observed in the food industry. This contributes to the provision of a wider range of cereal bakery products. The gradual increase in the consumption of brown bread is significant, but despite this, white bread remains a part of the typical Western diet. Studies showed high intake of carbohydrates increase TG levels by enhancing hepatic synthesis of very low-density lipoprotein (VLDL) and decrease activity of lipoprotein lipase. White bread consumption has been therefore associated with an unhealthy lifestyle. Objective. The aim of this study was to assess the influence of the consumption of gluten bakery products on lipids and inflammatory parameters of the probands. Material and Methods. The monitored group consisted of 30 probands from the general population. The average age of the monitored group was 29.7 years. The intervention dose consisted of a different combination of several types of bakery products containing gluten (bread, pastries, soft pastries) within the individual weeks of consumption, while the intervention lasted 6 weeks. An intervention dose of 150 to 200 g per day was set for women and 200 to 250 g per day for men. Biochemical blood parameters were determined using a fully automatic Biolis 24i Premium blood serum biochemical analyzer, by end-point photometry method. We tested the differences between the biochemic parameters by one-factor analysis of variance (ANOVA) and compared them by Tuckey’s Post Hoc Test. Results. The measurement of the lipid profile showed that the average levels of total cholesterol (TC) were above the reference value (

Objective To observe the cell viability, pyroptosis, inflammation and oxidative stress response of the preeclampsia (Preeclampsia, PE) model cells constructed using the human chorionic trophoblast cell line HTR-8/SVneo with low expression of microRNA-148a (miR-148a). Methods Human chorionic trophoblast cell line HTR-8/SVneo in the logarithmic growth phase were selected and divided into groups A, B, C, and D. Cells in the group A were transfected with miR-148a inhibitor (inhibiting miR-148a expression) for 24 h, followed by the addition of 100 ng/L LPS for 24 h (establishing a PE model cell); cells in the group B were transfected with NC inhibitor (blank control) and cultured for 24 h, followed by the addition of 100 ng/L LPS for 24 h; cells in the group C were cultured with 100 ng/L LPS for 24 h; cells in the group D were not treated. At 48 h of culture, qRT-PCR was used to detect miR-148a in cells of each group; CCK-8 was used to detect cell viability in each group; TUNEL method was used to calculate the apoptosis rate in each group; Western blotting was used to detect the apoptosis-related proteins Caspase-1, GSDMD, and NLRP3 in each group; ELISA was used to detect inflammatory factors (tumor necrosis factor-a [TNF-a], interleukin-1B [IL-1B], IL-6) and oxidative stress indicators (glutathione peroxidase [GSH], superoxide dismutase [SOD], and malondialdehyde [MDA]) in the supernatant of each group. Results Compared with the group D, the relative expression level of miR-148a was higher, and the OD values were lower at 24, 48, and 72 h of culture, the apoptosis rate was higher, and the relative expression levels of Caspase-1, GSDMD, and NLRP3 proteins in cells were higher in the group C (all P<0.05). Compared with the group B, the relative expression level of miR-148a was lower, and the OD values were higher at 24, 48, and 72 h of culture, the apoptosis rate was lower, and the relative expression levels of Caspase-1, GSDMD, and NLRP3 proteins in cells were low- er in the group A (all P<0.05). Compared with the group D, the levels of TNF-a, IL-1B, and IL-6 in the cell supernatant increased, the expression levels of GSH and SOD in cells were lower, while the expression of MDA increased in the group C (all P<0.05). Compared with the group B, the levels of TNF-a, IL-1B, and IL-6 in the cell supernatant were lower, the expression levels of GSH and SOD increased, and the expression of MDA decreased in the group A (all P<0.05). Conclusions The cell viability of the PE model cells constructed using HTR-8/SVneo with low expression of miR-148a is high, while the degree of pyroptosis, inflammatory response and oxidative stress response are low. MiR-148a may be one of the therapeutic targets of PE. [ABSTRACT FROM AUTHOR]

To explore the expression of inflammatory factors and TSP-1 in gingival crevicular fluid in patients undergoing orthodontic extraction, and the influencing factors of periodontal disease. Eighty patients admitted to our hospital from August 2020 to August 2023 for orthodontic treatment of extracted teeth were retrospectively analyzed, and gingival sulcus fluid samples were taken from all the patients before orthodontic treatment, 1 month after orthodontic treatment, 3 months after orthodontic treatment, and at the end of orthodontic treatment to detect the tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), and platelet reactive protein- 1 (TSP-1) expression levels. Subsequently, the patients were divided into periodontal disease group (n=36) and non-periodontal disease group (n=44) according to whether they suffered from periodontal disease during orthodontic treatment, compared the expression levels of TNF-琢, IL-1茁, IL-6, and TSP-1 of the patients in the two groups before orthodontic treatment and at the end of orthodontic treatment, and compared the general conditions of the patients in the two groups, and then analyzed the influence factors of periodontal diseases in patients with extracted teeth in orthodontics with the use of logistic regression model. Disease Influencing Factors. TNF-琢, IL-1茁, IL-6, and TSP-1 levels were elevated at 1 month and 3 months after orthodontic treatment in 80 patients with extracted teeth, and TNF-琢, IL-1茁, IL-6, and TSP-1 levels leveled off from 3 months to the end of orthodontic treatment, but were significantly higher than those before orthodontic treatment at 1 month, 3 months, and at the end of orthodontic treatment (P<0.05); there were significant differences in the expression levels of TNF-琢, IL-1茁, IL-6, and TSP-1 in patients in the periodontal diseases group compared to those in the non periodontal diseases group, and the expression levels in the periodontal diseases group were significantly higher than those in the non periodontal diseases group (P<0.05). There were significant differences in the expression levels of TNF-琢, IL-1茁, IL-6, and TSP-1 between patients in the pre-orthodontic and post-orthodontic groups, and the periodontal disease group was significantly higher than the non-periodontal disease group (P<0.05); there were no significant differences in the comparison of gender, age, and BMI between patients in the periodontal disease group and the non-periodontal disease group (P>0.05), and there were no significant differences in the duration of orthodontic treatment, number of extractions, oral cavity, oral cavity, and oral health of patients in the periodontal disease group and the non-periodontal disease group (P<0.05). number, orthodontic method, and oral cleanliness were compared significantly (P<0.05); logistic regression analysis showed that TNF-琢, IL-1茁, IL-6, TSP-1, orthodontic method, and oral cleanliness were independent risk factors for periodontal disease in patients with extracted teeth and orthodontic treatment (P<0.05). Inflammatory factors of gingival crevicular fluid and TSP-1 levels increased significantly in orthodontic patients with prolonged orthodontic time, and TNF-琢, IL-1 茁, IL-6, TSP-1, orthodontic mode and oral cleanliness were independent risk factors for periodontal disease in orthodontic patients. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the inflammatory reaction and the ability to induce mineralization activity of a new repair material, NeoPUTTY (NPutty; NuSmile, USA), in comparison with Bio‐C Repair (BC; Angelus, Brazil) and MTA Repair HP (MTA HP; Angelus, Brazil). Methodology: Polyethylene tubes were filled with materials or kept empty (control group, CG) and implanted in subcutaneous tissue of rats for 7, 15, 30, and 60 days (n = 6/group). Capsule thickness, number of inflammatory cells (ICs), fibroblasts, collagen content, and von Kossa analysis were performed. Unstained sections were evaluated under polarized light and by immunohistochemistry for osteocalcin (OCN). Data were submitted to two‐way anova followed by Tukey's test (p ≤.05), except for OCN. OCN data were submitted to Kruskal–Wallis and Dunn and Friedman post hoc tests followed by the Nemenyi test at a significance level of 5%. Results: At 7, 15, and 30 days, thick capsules containing numerous ICs were seen around the materials. At 60 days, a moderate inflammatory reaction was observed for NPutty, BC while MTA HP presented thin capsules with moderate inflammatory cells. In all periods, NPutty specimens contained the highest values of ICs (p <.05). From 7 to 60 days, the number of ICs reduced significantly while an increase in the number of fibroblasts and birefringent collagen content was observed. At 7 and 15 days, no significant difference was observed in the immunoexpression of OCN (p >.05). At 30 and 60 days, NPutty showed the lowest values of OCN (p <.05). At 60 days, a similar immunoexpression was observed for BC and MTA HP (p >.05). In all time intervals, capsules around NPutty, BC, and MTA HP showed von Kossa‐positive and birefringent structures. Conclusions: Despite the greater inflammatory reaction promoted by NeoPutty than BC and MTA HP, the reduction in the thickness of capsules, the increase in the number of fibroblasts, and the reduction in the number of ICs indicate that this bioceramic material is biocompatible Furthermore, NeoPutty presents the ability to induce mineralization activity. [ABSTRACT FROM AUTHOR]

The purpose of this paper was to investigate the anti-inflammatory and anti-angiogenic activities of sulfated polysaccharide from C. tomentosum (PCT) using carrageenan (CARR)-induced paw edema in a rat model and anti-vasculogenic activity on a chorioallantoic membrane assay (CAM) model. Based on in vitro tests of anti-radical, total antioxidant, and reducing power activities, PCT presents a real interest via its antioxidant activity and ability to scavenge radical species. The in vivo pharmacological tests suggest that PCT possesses anti-inflammatory action by reducing paw edema and leukocyte migration, maintaining the redox equilibrium, and stabilizing the cellular level of several pro-/antioxidant system markers. It could significantly decrease the malondialdehyde levels and increase superoxide dismutase, glutathione peroxidase, and glutathione activities in local paw edema and erythrocytes during the acute inflammatory reaction of CARR. PCT pretreatment was effective against DNA alterations in the blood lymphocytes of inflamed rats and reduced the hematological alteration by restoring blood parameters to normal levels. The anti-angiogenic activity results revealed that CAM neovascularization, defined as the formation of new vessel numbers and branching patterns, was decreased by PCT in a dose-dependent manner, which supported the in silico bioavailability and pharmacokinetic findings. These results indicated the therapeutic effects of polysaccharides from C. tomentosum and their possible use as anti-proliferative molecules based on their antioxidant, anti-inflammatory, and anti-angiogenic activities. [ABSTRACT FROM AUTHOR]

Objective To explore the clinical efficacy of acetylcysteine solution retained perfusion inhalation treatment under electronic bronchoscopy in children with severe bacterial pneumonia. Methods From January 1，2021 to December 31，2022，86 children with severe bacterial pneumonia treated in the Department of Respiratory Medicine of Kunming Children’s Hospital were randomly divided into a control group (n = 43) and a study group (n = 43) . The children in the control group received electronic bronchoscopy under physiological saline pulmonary alveolar lavage treatment. The study group received acetylcysteine solution treatment retained after the end of the pulmonary lavage treatment. The clinical treatment effects， inflammatory indicators， tidal breathing function，and adverse reactions of the two groups were compared. Results After treatment，compared with control group，the hospitalization time，cough disappearance time and comorbidities disappearance time of children in study group were significantly shortened (P < 0.05), and the total effective rate of study group was significantly higher than that of control group (P < 0.05) . The levels of white blood cell count，procalcitonin，C-reactive protein， interleukin-6，and tumor necrosis factor-α of study group were significantly lower than those of control group (P < 0.05) . The tidal volume per kilogram of body weight，peak time ratio，and peak volume ratio levels of study group were significantly higher than those of control group (P < 0.05) .There was no statistically significant difference in the adverse drug reactions between two groups （P > 0.05）. Conclusion Under electronic bronchoscopy，preserving perfusion and inhaling acetylcysteine solution can significantly improve the clinical symptoms， inflammatory indicators，and lung function of children with severe bacterial pneumonia，and it is relatively safe [ABSTRACT FROM AUTHOR]

Sevoflurane exposure can result in neurotoxicity especially among children, which remains an important complication after surgery. However, its related mechanisms remain unclear. Here, we investigated the biological roles of SHARPIN in sevoflurane-induced neurotoxicity. As detected by qPCR, Western blotting and immunohistochemical staining, SHARPIN and HMGB1 expression was elevated in sevoflurane-stimulated mice as compared with the control mice. SHARPIN depletion attenuated hippocampus injury, repressed the expression of HMGB1 and M1-like macrophage markers (iNOS, TNF-α, IL-1β, IL-6), but enhanced the expression of M2-like macrophage markers (ARG-1, IL-10). GST pull-down and Co-IP assays demonstrated that SHARPIN directly interacted with HMGB1 to enhance HMGB1 expression in SH-SY5Y cells. The inhibitory effects of SHARPIN silencing on inflammatory reaction and M1-like macrophages were counteracted by HMGB1 overexpression. Finally, SHARPIN-HMGB1 pathway affected neuroinflammation triggered by sevoflurane via modulating macrophage polarization. Collectively, our data suggested that SHARPIN stimulated sevoflurane-induced neurotoxicity via converting M2-like macrophages to M1-like macrophages by enhancing HMGB1 expression. SHARPIN intervention may be a promising therapeutic method to relieve sevoflurane-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Background: This study investigated the contact between adult dental pulp stem cells (DPSCs) and carbamide peroxide (CP), a bleaching agent that is a popular choice for at-home whitening products, using an in vitro model. Objectives: The aim of this study was to evaluate the impact of exposure to different concentrations and timings of a commonly used peroxide-based home tooth-whitening product on DPSCs. Materials and methods: Human DPSCs obtained from impacted third molars were cultured and exposed to various concentrations of carbamide peroxide (0.1%, 0.5%, and 1%). The effects of CP on DPSC proliferation and apoptosis were investigated by MTT assay and flow cytometry. Migration was investigated by micrographs of wound healing. An enzyme-linked immunosorbent assay (IL-6 and IL-8) was used to investigate the CP-stimulated cytokine production of DPSCs. Each experiment was performed three times with independent batches of DPSCs. Statistical analysis of the collected data was performed using one-way and two-way ANOVAs with the significance threshold set at p < 0.05. Tukey's post hoc multiple comparison test was used to identify differences between groups. Results: Cell viability and adherence were lower in the CP-exposed cells compared to the non-stimulated cells, probably due to increased cell death (** p ≤ 0.01, **** p ≤ 0.0001). CP-stimulated DPSCs exhibited a dose-dependent release of IL-6 and IL-8 (**** p ≤ 0.0001). CP did not affect wound healing at any concentration tested. Conclusions: Human DPSCs were able to sense CP. Consequently, CP contributed significantly to cell apoptosis and local inflammatory responses through cytokine release. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD), the most common form of dementia, has a complex pathogenesis. The number of AD patients has increased in recent years due to population aging, while a trend toward a younger age of onset has arisen, imposing a substantial burden on society and families, and garnering extensive attention. DNA methylation has recently been revealed to play an important role in AD onset and progression. DNA methylation is a critical mechanism regulating gene expression, and alterations in this mechanism dysregulate gene expression and disrupt important pathways, including oxidative stress responses, inflammatory reactions, and protein degradation processes, eventually resulting in disease. Studies have revealed widespread changes in AD patients' DNA methylation in the peripheral blood and brain tissues, affecting multiple signaling pathways and severely impacting neuronal cell and synaptic functions. This review summarizes the role of DNA methylation in the pathogenesis of AD, aiming to provide a theoretical basis for its early prevention and treatment. [ABSTRACT FROM AUTHOR]

Abdominal aortic aneurysm (AAA) is a common disease in the elderly, with an increasing incidence rate, easy rupture, high mortality, and no effective drugs to slow down the development of AAA. The pathogenesis of AAA is closely related to extracellular matrix degradation, apoptosis of vascular smooth muscle cells and inflammation. It has been found that arachidonic acid derivatives, especially prostaglandins such as prostaglandin E2 (PGE2), prostaglandin D2 (PGD2) and thromboxane A2(TXA2), play important roles in the development of AAA. Therefore, this review discusses the mechanism of arachidonic acid derivatives in the development of AAA, as well as the latest research progress of the drugs, to provide ideas for the treatment of AAA and the discovery of new drug targets. [ABSTRACT FROM AUTHOR]

Canine visceral leishmaniasis (CVL), caused by the protozoan Leishmania infantum, affects several organs, including the skin. Dogs are considered the major domestic reservoir animals for leishmaniasis, and through their highly parasitized skin, they can serve as a source of infection for sandfly vectors. Therefore, studies of the skin parasite–host relationship can contribute to the understanding of the infectious dissemination processes of parasites in the dermis and help to identify targets for diagnosis and treatment. Thus, the aim of this study was to evaluate the association of anatomical vascular differences and Leishmania-induced vascular morphological changes with clinical signs and parasite load by analyzing the ear and abdominal skin from dogs naturally infected with L. infantum. Paired samples of ear and abdominal skin from L. infantum-positive dogs (n = 26) were submitted for histological and immunohistochemistry analyses. The ear skin samples showed a more intense and more diffusely distributed granulomatous inflammatory reaction, a higher number and larger diameter of blood vessels, increased parasite load, higher expression of VEGF+ (vascular endothelial growth factor) and MAC 387+ (calprotectin) recently infiltrating cells, and more intense collagen disruption compared to the abdominal skin samples. Intracellular amastigotes were observed in blood vessels and inside endothelial cells and were diffusely distributed throughout the dermis in the ear skin samples. The NOS2/MAC387+ cell ratio was lower in the ear skin samples than in those of the abdomen, suggesting that in the ear dermis, the inflammatory infiltrate was less capable of producing NO and thereby control the parasite load. Together, these findings indicate how parasites and immune cells are distributed in the skin and suggest an important role for dermal vascularization in cellular influx and thereby in parasite dissemination through the skin of naturally infected dogs. [ABSTRACT FROM AUTHOR]

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Ischemic stroke is a common acute cerebrovascular disease in clinical practice, which poses a severe threat to human health. In recent years, with deepening understanding of ischemic stroke, significant progress has been made in the diagnosis and treatment. However, current treatments for ischemic stroke are partially limited due to extremely complex pathological mechanisms. Studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of ischemic stroke. Therefore, modulation of mitochondrial function through mitochondrial dynamics is essential to ameliorate the damage of cerebral ischemic neuronal cells. In this article, the molecular mechanism of mitochondrial dynamics and its role in ischemic stroke were reviewed, aiming to provide useful reference for the treatment of ischemic stroke. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of L-carnitine supplementation in uremic patients receiving hemodialysis. Methods Totally100 uremic patients undergoing hemodialysis were randomly divided into the control group and observation group according to the random number table, with 50 cases in each group. All patients received hemodialysis and routine nursing management, and patients in the observation group received intravenous drip of L-carnitine after hemodialysis treatment. The clinical effect of the hemodialysis treatment was evaluated, and changes of renal function indexes, nutrition indexes, serum inflammatory factors and complications were compared between two groups. Results The overall effective rate was 98. 00%(49/50)in the observation group and 86. 00%(43/50)in the control group, with no significant difference (P＞0. 05). Compared with patients in the controlgroup, patients in the observation group had a higher Ccr and lower level of Scr and BUN after treatment(P＜0. 05). The levels of PA, TRF, ALB and Hb in the observation group were higher than those in the control group after treatment(P＜0. 05). The levels of IL-6, CRP and TNF-α in the observation group were lower than those in the control group after treatment(P＜0. 05). There was no significant difference in incidence of complication between two groups(P＞0. 05). Conclusion The application of L-carnitine in hemodialysis treatment for uremic patients can improve the renal function and nutritional status, reduce the inflammatory reaction and complications, and helps to ensure the efficacy of hemodialysis treatment (目的 探讨左卡尼汀对尿毒症血液透析患者营养指标及炎症状态的影响。方法 选取2019年1月—2021年6月医院收治的尿毒症患者100例, 采用随机数字表法分为对照组和观察组, 各50例。两组均实施常规血液透析治疗和护理, 观察组于每次静脉透析治疗后静脉滴注左卡尼汀。评价两组治疗效果, 对比两组肾功能指标、营养指标、血清炎性因子指标、并发症发生情况。结果 观察组总有效率为98. 00%(49/50), 高于对照组的86. 00%(43/50), 差异无统计学意义(P＞0. 05)。治疗后, 观察组内生肌酐清除率(Ccr)高于对照组, 血肌酐(Scr)和尿素氮(BUN)水平低于对照组, 差异有统计学意义(P＜0. 05)。治疗后, 观察组前清蛋白(PA)、转铁蛋白(TRF)、白蛋白(ALB)、血红蛋白 (Hb)水平高于对照组, 差异有统计学意义(P＜0. 05)。治疗后, 观察组白细胞介素-6(IL-6)、C反应蛋白(CRP)和肿瘤坏死因子-α(TNF-α)水平低于对照组, 差异有统计学意义(P＜0. 05)。两组并发生发生率差异无统计学意义(P＞0. 05)。结论 尿毒症患者血液透析治疗中应用左卡尼汀, 能改善患者营养状况, 减轻炎症反应, 降低并发症风险, 确保透析治疗效果。)