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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]

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]

We aimed to explore the association between obesity and depression and the role of systemic inflammation in older adults. Adults ≥ 65 years old (n = 1,973) were interviewed at baseline in 2018 and 1,459 were followed up in 2021. General and abdominal obesity were assessed, and serum C-reactive protein (CRP) levels were measured at baseline. Depression status was assessed at baseline and at follow-up. Logistic regression was used to analyze the relationship between obesity and the incidence of depression and worsening of depressive symptoms, as well as the relationship between obesity and CRP levels. The associations of CRP levels with the geriatric depression scale, as well as with its three dimensions, were investigated using multiple linear regressions. General obesity was associated with worsening depression symptoms and incident depression, with an odds ratio (OR) [95% confidence interval (CI)] of 1.53 (1.13–2.12) and 1.80 (1.23–2.63), especially among old male subjects, with OR (95% CI) of 2.12 (1.25–3.58) and 2.24 (1.22–4.11), respectively; however, no significant relationship was observed between abdominal obesity and depression. In addition, general obesity was associated with high levels of CRP, with OR (95% CI) of 2.58 (1.75–3.81), especially in subjects free of depression at baseline, with OR (95% CI) of 3.15 (1.97–5.04), and CRP levels were positively correlated with a score of specific dimension (life satisfaction) of depression, P < 0.05. General obesity, rather than abdominal obesity, was associated with worsening depressive symptoms and incident depression, which can be partly explained by the systemic inflammatory response, and the impact of obesity on depression should be taken more seriously in the older male population. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Numerous studies show association of particular matter (PM) in air pollution with cardiovascular dysfunction, and increased morbidity and mortality. The main mechanisms of this adverse effect involve increasing oxidative stress, inflammatory responses, and genotoxicity. Several recent studies investigated the ability of PM2.5 to cause myocardial injury in animal models using various methods, such as intratracheal instillation, intraperitoneal injection or tail vein injection. The purpose of this study is to explore the PM2.5-induced myocardial inflammatory reaction in rats through the new technology of multi-functional aerosol concentration and enrichment system. MATERIALS AND METHODS: Thirty Wistar rats were divided into two groups, 15 in each group. In the exposure group, PM2.5 multi-functional aerosol concentration and enrichment system was used for PM2.5 online oral and nasal exposure (5 times a week, 4 hours exposure, for the duration of 3 months). Histopathological examination of the left ventricular myocardial tissue of both groups was done using hematoxylin and eosin (H&E) staining. Ultrastructural changes of the heart specimens were assessed using electron microscopy. The levels of CRP and ICAM-1 were detected by immunohistochemistry. RESULTS: Compared with the control group, myocardial tissue of the exposure group exhibited edema, widened myocardial space and infiltration of inflammatory cells. There was nuclear pyknosis, mitochondrial membrane and spinal fusion, rough endoplasmic reticulum expansion, degranulation and cell swelling in the exposed group. The area of CRP positive staining in the exposed group was 3.7-fold higher than that in the control group (p < 0.05), and the ICAM-1 positive staining area of the exposed group was 12-fold higher than that of the control group (p < 0.05). CONCLUSIONS: Prolonged exposure to PM2.5 inhalation promotes significant upregulation of ICAM-1 and CRP expression in myocardial tissues, ultrastructural alterations in myocardial cells, and influx of inflammatory cells. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the regulatory role of miR-135a-5p/CXCL12/JAKSTAT signaling axis in inflammatory response after myocardial infarction (MI). MATERIALS AND METHODS: With the construction of mouse model with MI by ligation of left descending coronary artery, modeling mice were subdivided into sh-NC group, sh-CXCL12 group, agomir-NC group, miR-135a-5p agomir group and miR-135a-5p-agomir+pcDNA-CXCL12 with intravenous injection of corresponding adenovirus, and no modeling was made for mice in the sham operation group. Simulation of MI in vivo was realized by hypoxia model in vitro, with the establishment of groups including mimic-NC group, miR-135a-5p mimic group, inhibitor- NC group, miR-135a-5p inhibitor group, sh-NC group, sh-CXCL12 group, oe-NC group, oe-CXCL12 group, mimic NC+oe-NC group, miR- 135a-5p mimic+oe-NC group, and miR-135a-5p mimic+oe-CXCL12 group. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the level of miR-135a-5p, CXCL12, TNF-a, IL-1ß and IL-6, and Western blot were further performed to detect the mRNA and protein expression of JAK2/p-JAK2 and STAT3/ p-STAT3, respectively. Hematoxylin-eosin (HE) staining and terminal deoxynucleotidyl transferase- mediated dUTP-biotin nick end labeling (TUNEL) assay were used to evaluate MI in mice. Dual-Luciferase reporter assay was used to verify the targeting relationship between miR- 135a-5p and CXCL12. Annexin V-fluorescein isothiocyanate/propidium iodide (V-FITC/PI) double staining analysis by flow cytometry was used to detect apoptosis. RESULTS: After hypoxia of myocardial cell line H9c2 for 24 h, there were increased expression of CXCL12, decreased expression of miR-135a-5p, increased number of apoptotic cells, as well as upregulated levels of TNF-a, IL-1ß and IL-6 (all p<0.05). Meanwhile, similar results were found in the myocardial tissues. Dual-Luciferase reporter assay indicated that miR-135a-5p could target the expression of CXCL12. Transfection of miR-135a-5p mimic or sh-CXCL12 could reduce the number of apoptotic myocardial cells and inhibit the level of TNF-a, IL-1ß and IL-6 (all p<0.05). Furthermore, miR-135a-5p mimic or sh-CXCL12 could result in the suppressed expression of p-JAK2 and p-STAT3 (all p<0.05). Compared with miR-135a-5p mimic +DMSO group, the expression of JAK2 and STAT3 in miR-135a- 5p mimic +RO8191 group had no significant change (p>0.05); the expression of p-JAK2 and p-STAT3 was increased (all p<0.05), suggesting that miR-135a-5p negatively regulated the expression of CXCL12 and inhibited the activation of JAK-STAT signaling pathway. In addition, for further verification, experiments carried out in sh-NC group, sh-CXCL12 group, agomir-NC group and miR-135a-5p agomir group found that sh-CXCL12 and miR- 135a-5p agomir resulted in decreased area of MI decreased, the number of apoptotic cells, the expression of p-JAK2 and p-STAT3 (all p<0.05); while compared with miR-135a-5p-agomir group, miR-135a-5p-agomir+pcDNA-CXCL12 group showed increased area of MI decreased, the number of apoptotic cells, the expression of p-JAK2 and p-STAT3 (all p<0.05). CONCLUSIONS: Inhibition of miR-135a-5p/CXCL12/JAK-STAT signaling axis can reduce inflammatory reaction and apoptosis after MI, and hence contribute to the improvement of the degree of myocardial injury. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the effects of inflammatory response on renal function and TGF-β1 pathway of rats with aging-related kidney damage by upregulating the CD36 expression. MATERIALS AND METHODS: A total of 70 pathogen free (PF) Sprague-Dawley (SD) male rats were enrolled. The rats injected with normal saline and D-galactose were assigned to a control group and a model group, respectively. Those injected with both D-galactose and different concentrations of casein were assigned to casein A, B, and C groups accordingly, and 16 rats injected with D-galactose and with CD36 gene knocked out were assigned to a treatment group. The following methods were employed to determine the following factors of the rats: ELISA for serum inflammatory factors, Western blot for CD36 in kidney tissues, Real Time-PCR for TGF-β1, and Smad (2, 3, and 7) mRNA, radioimmunoassay for hyaluronic acid (HA) and laminin (LN), and colorimetry for the expression quantity of plasma superoxide dismutase (SOD) and malondialdehyde (MDA). An automatic biochemical analyzer was used to determine blood, urine, and renal function indexes. RESULTS: After successful modeling, the model group showed significantly higher inflammatory indexes than the control group. The relative expression of CD36 in the model group was significantly higher than that in the control group and treatment group, and significantly lower than that in the casein groups. Both inflammatory indexes and relative expression of CD36 increased with the increase of casein concentration in the casein groups. Groups with severer inflammatory response showed higher renal function indexes, and higher expression of TGF-β1, Smad2, Smad3, HA, LN, and MDA, and those with decreased CD36 level showed lower renal function index levels. The Smad7 expression and SOD were contrary. CONCLUSIONS: Inflammatory stress can promote the CD36 expression in renal tissues of aging rats and oxidative stress and affect TGF-β1/ Smad pathway, thus aggravating renal fibrosis and renal damage in rats. [ABSTRACT FROM AUTHOR]

Highlights • This is the first article which is conducted on the effects of Ganoderma triterpenoids on liver damage in cadmium poisoning animals. • Cadmium leaks cause oxidative damage and inflammatory reactions in chicken livers. • GT can reduce the content of Cd in the liver of chicken, thereby increasing antioxidative capacity and reducing the tissue´s inflammatory status. Abstract Several studies have been conducted on liver damage caused by cadmium, but few on the protective effects of Ganoderma triterpenoids against liver damage due to cadmium. This experiment was designed to evaluate the protective effects of Ganoderma triterpenoids on the liver damage induced by cadmium in chickens. Eighty healthy seven-day-old Hyline male egg-laying chickens were randomly divided into four groups with 20 chickens in each group. All the experiments were carried out in triplicate. The control group (K group) was fed a basal diet, the Cadmium group (Cd group) was fed a basal diet with 140 mg/kg of CdCl 2 , the Ganoderma triterpenoids treatment group (Cd + GT group) was fed with a full-fodder diet containing 140 mg/kg of CdCl 2 and 0.5 mL of Ganoderma triterpenoids solution (20 mg/mL), and the Ganoderma triterpenoids group (GT group) was fed a basal diet and 0.5 mL of Ganoderma triterpenoids solution (20 mg/mL). At the 20th, 40th, and 60th days, fifteen chickens were randomly selected for euthanasia in each group. Livers were quickly removed and stored on ice. Some indicators, such as the cadmium content in the liver, antioxidant enzymes (superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px)) activities, malondialdehyde (MDA) content, and inflammatory factors(Tumor necrosis factor alpha (TNF-α), interleukin (IL-1β and IL-6)), heat shock protein (HSP27, 40, 60, 70, and 90) mRNA levels, and protein levels of heat shock proteins (HSP60, 70, and 90) were detected, and chicken liver pathology was taken for each group every 60 days. The results showed that cadmium exposure caused accumulation of cadmium in liver tissue, inhibited antioxidant enzyme activity, and increased MDA content, inflammatory cytokines (TNF-α IL-1β and IL-6), and heat shock protein (HSP27, 40, 60, 70, and 90) mRNA levels, and heat shock protein (HSP60, 70, and 90) levels, with severe tissue damage and inflammatory infiltrates. Ganoderma triterpenoids not only reduced the accumulation of cadmium in the chicken liver, but also significantly increased the activities of antioxidant enzymes which is inhibited by cadmium, reduced the content of MDA, mRNA expressions of inflammatory cytokines (TNF-α IL-1β and IL-6), and heat shock proteins (HSP27, 40, 60, 70, and 90), and protein levels of heat shock proteins (HSP60, 70, and 90). Simultaneously, pathological tissue sections showed that the pathological damage of the liver tissue was significantly reduced. The results showed that Ganoderma triterpenoids can significantly reduce the accumulation of cadmium in the liver of chicken, thereby reducing oxidative stress and inflammation. [ABSTRACT FROM AUTHOR]

Celecoxib is the most recent non steroidal anti-inflammatory analgesic, and has been gradually used in the treatment of acute pain, rheumatism and osteoarthritis. This paper analyzes the analgesic effect of celecoxib in the treatment of knee osteoarthritis and put forward a new mechanism of knee joint extensor reconstruction assisted by bone anchor. The experimental group was given celecoxib 200 mg/time and 1 time /d. The results showed that VAS (Visual Analogue Scale) decreased gradually in both groups on the 1st, 3rd and 7th day of treatment and VAS in experimental group was lower than that in control group at the same time point (P<0.05). At the 1 year follow-up, experience group had a significant improvement on the Lysholm (69.33 ± 8.38 preoperatively and 88.65 ± 12.93 postoperatively) and Kujula (69.33 ± 8.38 preoperatively and 88.65 ±12.93 postoperatively) knee scores (P<0.05). The results showed that celecoxib had a good analgesic effect in patients with knee osteoarthritis and reducing the release of inflammatory factors may be its mechanism. [ABSTRACT FROM AUTHOR]

Background: Genistein was reported to adversely influence fetal development although this is yet to be fully understood as a mechanism. Methods: In this study, pregnant rats were divided into control (Cont.) and genistein force-fed (2-mg/kg and 4-mg/kg) groups. Each group was divided further into five subgroups: GD-0, GD-6, GD-13, GD-18, and GD-20 based on the terminal gestational day (GD). On the respective terminal GD, the rats were sacrificed and blood samples and amniotic fluid were carefully collected and separated and placenta homogenates were prepared. These samples were evaluated for oxidative stress and inflammatory reaction. The weights of embryonic implant and placenta tissue were also recorded. Heat shock protein (Hsp) (60 and 90), corticosterone, and oxidative stress biomarkers were determined in all the samples. Results: Fetal and placental weights in all genistein-exposed groups were significantly decreased. A fluctuation in the level of the Hsp was recorded with a significant decrease recorded in Hsp90 level in the placenta and amniotic fluid towards GD-20 along with a concomitant increase in the corticosterone level in the amniotic fluid in all genistein groups compared to control. Maternal serum at GD-18 and GD -20 recorded a significant increase in antioxidant level (SOD, GSH, CAT) in all genistein-exposed groups. However, these antioxidants were significantly reduced in the placenta and the amniotic fluid compared to control. Conclusions: Genistein enhances the placenta function in attenuating the risk of oxidative stress in the amniotic fluid and deferentially suppressed inflammatory activities in the placenta during early gestation and towards late gestation period. [ABSTRACT FROM AUTHOR]

Chronic cadmium (Cd) exposure causes severe adverse health effects on the human body, especially the kidney tissue. Studies have demonstrated oxidative stress to be involved in renal pathological variations after exposure to Cd, but few effective treatments are available for the disease yet. Therefore, the present study was carried out to investigate the potential therapeutic intervention and its underlying molecular mechanisms of melatonin (MT), a natural antioxidant with multiple biological activities, against renal injury caused by Cd exposure in mice. C57BL/6 male mice (eight-week-old) were intragastrically administered with CdCl 2 , MT, or both for 30 days. Biochemical analysis showed that MT intervention significantly improved the SOD, GSH, and CAT activities while markedly decreasing the kidney MDA content of the mice exposed to Cd. Histological examination indicated that Cd exposure resulted in the atrophy of the renal glomerular, the degeneration and dilation of tubules, and the accumulation of fibrocytes. By contrast, MT administration effectively ameliorated the histological outcome of the injured kidney tissue. Moreover, administrating MT significantly inhibited proinflammatory cytokines TNF-α and iNOS expression in Cd-treated mice. Further, MT treatment markedly suppressed the expressions of renal fibrosis-related factors TGF-β1, α-SMA, and collagen Ⅰ in the injured renal tissue and the accumulation and development of renal fibrosis. In addition, the administration of MT significantly reduced the expression of caspase-3 and cell apoptotic death in the kidney tissue of Cd-exposed mice. In all, the data showed that MT has a compelling therapeutic potential in alleviating the pathological variations of renal injury caused by Cd exposure. • Oxidative stress might be a vital mediator for progressive pathophysiological changes of Cd-induced renal injury. • Renal fibrosis is involved in Cd-induced nephrotoxicity. • MT attenuates Cd-induced nephropathy by regulating oxidative stress, inflammatory response, cell apoptosis, and fibrosis. • Antioxidant therapeutics provided a novel insight into the mechanisms of Cd-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

Summary Introduction There is no consensus on the ideal graft for medialization surgery of the vocal folds in the literature. One of the most favorable proposals is the use of autologous fascia, which seems limited by the lack of information regarding the integration of grafted tissue. Our study aims to evaluate the degree of fully engrafted fascia integration in the vocal fold lamina propria of dogs. Materials and Methods Fourteen adult mongrel dogs that underwent intravenous general anesthesia were selected and kept under spontaneous ventilation. A fascia lata fragment of 4 cm 2 was obtained from the right leg of each dog. The dogs underwent laryngoscopy; a 3 mm incision was made in the vocal process, next to the vestibular process, and the fascia was grafted into the right vocal fold. The left vocal fold was used as a control. The animals were divided into two groups: group A, evaluated after 2 months of the procedure, and group B, evaluated after 6 months of the procedure. Histologic analysis was made semiquantitatively regarding the presence of inflammatory reaction, fibrosis, and neovascularization. Results Our final studied group comprised 12 dogs. Microscopic examination of the larynx revealed the absence of any detectable inflammation in the incision site. The lamina propria of the grafted vocal fold showed identifiable compact, thick, and eosinophilic collagen bands. The surrounding tissue showed thin collagen bands with some organization, similar to the contralateral vocal fold. Conclusion The grafted fascia integrates into the vocal fold lamina propria and seems not to cause inflammatory reaction response. [ABSTRACT FROM AUTHOR]

Objective: To investigate the postoperative inflammatory reaction, stress reaction and immune response of laparoscopic surgery and laparotomy for acute gastric perforation. Methods: Forty-four patients with acute gastric perforation receiving emergency surgery in our hospital from May 2012 to December 2015 were selected and retrospectively analyzed. Among these patients, there were 19 patients treated with laparoscopic surgery (LS group) and 25 patients treated with laparotomy (laparotomy group). At the first day after surgery, their serums were collected and the indexes of inflammatory reaction and stress reaction were detected. Mononuclear cells and red blood cells in peripheral blood were collected and detected for the immune function indexes. Results: At day 1 after surgery, the contents of serum interleukin-1β (IL-1β), IL-2, IL-6, IL-8, IL-10, cortisol, norepinephrine, epinephrine, renin and angiotensin-II of patients in the LS group were all significantly lower than those of the laparotomy group; fluorescence intensities of CD3, CD4, CD16 and CD56 of mononuclear cells in peripheral blood were all obviously higher than those of the laparotomy group; and the numbers of red blood cell C3bR and immune complex resette and the fluorescence intensities of complement receptor type 3, CD58 and CD59 were obviously higher than those of the laparotomy group. Conclusions: Emergency laparoscopic surgery used to treat acute gastric perforation shows slight postoperative inflammatory reaction and stress reaction and presents weak nonspecific immune response, specific immune response and erythrocyte immune response, which makes less trauma than laparotomy. [ABSTRACT FROM AUTHOR]

Objective: To investigate the different effects on evacuation of hematoma, the severity of nerve injury, inflammatory reaction and oxidative stress response in the treatment of acute intracerebral hemorrhage by using minimally invasive puncture and drainage assisted with alteplase or urokinase. Methods: A total of 114 patients with acute intracerebral hemorrhage treated with minimally invasive puncture and drainage in our hospital from May 2012 to October 2015 were retrospectively analyzed and divided into alteplase group and urokinase group, which received adjuvant therapy with alteplase and urokinase, respectively. Before and after treatment, CT was used for scanning, and the volume of hematoma and edema and the distance of midline shift were examined. After treatment, serum was collected for detecting the contents of molecular markers of nerve injury, inflammatory reaction and oxidative stress response. Results: On the 3rd day after treatment, the volume of hematoma and edema and the distance of midline shift in minimally invasive group were significantly lower than those of craniotomy group, and incidence of intracranial infection was lower than that of craniotomy group. There was no significant difference of rebleeding incidence compared to craniotomy group. The serum contents of osteopontin, S100β, glial fibrillary acidic protein, neuron-specific enolase, myelin basic protein, neuropeptide Y, ischemia modified albumin, tumor necrosis factor alpha, interleukin-1β, interleukin-6, interleukin-8, soluble intercellular adhesion molecule-1, highmobility group protein 1, malonaldehyde, advanced oxidation protein products and 8-hydroxy-2'-deoxyguanosine urine of patients from alteplase group were significantly lower than those of urokinase group. The content of total antioxidant capacity was obviously higher than that of urokinase group. Conclusions: As for the effect on evacuation of hematoma and also the ameliorative effect on nerve injury, inflammatory reaction and oxidative stress response in treatment of acute intracerebral hemorrhage, minimally invasive puncture and drainage assisted with alteplase was superior to adjuvant therapy with urokinase. [ABSTRACT FROM AUTHOR]

Necrotizing enterocolitis (NEC) is a severe disease in newborns, this study aimed to investigate the protective effect of dimethyl fumarate (DMF) on NEC and its possible mechanism. In vivo, the mice were divided into the control, NEC, and NEC+DMF group. The NEC model was established by artificial feeding, hypoxic for 4 days, and lipopolysaccharide (LPS) stimulation on day 2 and day 3. DMF (25 mg/kg/d) was administered to NEC mice on day 1 and day 3. On the 11th day, the blood and intestinal tissues of mice were taken for enzyme-linked immunosorbent assay (ELISA), pathological examination, quantitative real-time PCR (RT-qPCR), Western blot, and immunohistochemical (IHC) detection. In vitro , human colorectal cells (FHC) were induced by LPS (100 ng/mL) and was divided into the control, LPS, and LPS+DMF group. The effect of DMF (20 μM) on cell viability and TLR4 signal transduction was detected by MTT and RT-qPCR, respectively. Compared to the NEC mice, DMF attenuated NEC-induced weight loss and abdominal distension diarrhea in mice, and alleviated NEC-induced intestinal pathological injuries. In addition, DMF reduced the expression of IL-6, IL-1β, TNF-α, NF-κB, and TLR4 in NEC mice intestinal tissues. Furthermore, DMF inhibited NEC-induced intestinal cell apoptosis as well as the protein expression of BCL2-Associated X (BAX), caspase-3, caspase-9, and increased Bcl-2 (B-cell lymphoma-2) expression. In vitro , DMF improved cell viability, and restrained NF-κB and TLR4 expression in LPS-induced NEC cells. DMF has a protective effect against intestine damage of NEC, which is related to the inhibition of the TLR signaling pathway, alleviating the inflammatory response. • Dimethyl fumarate (DMF) attenuated Necrotizing enterocolitis(NEC)-induced weight loss and abdominal distension diarrhea in mice model. • DMF reduced the release of IL-6, IL-1β, and TNF-α in NEC mice intestinal tissues. • DMF attenuated intestinal inflammation of NEC mice via TLR signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of anisodamine combining with conventional therapy on the degree of lung injury and inflammatory reaction of patients with acute pulmonary contusion. Methods A total of 48 patients with acute pulmonary contusion treated in our hospital emergency department from April 2011 to October 2015 were enrolled as the research object and were divided into experimental group and control group by using a method of random number table. Experimental group received anisodamine combining with conventional therapy and control group received conventional therapy. In the process of the treatment, the mechanical ventilation time, hospital stays in intensive care unit and the number of cases developed into acute respiratory distress syndrome and multiple organ dysfunction syndromes of patients in two groups were observed. Oxygenation indexes of patients were respectively calculated on Days 1, 2 and 3 after treatment. The contents of inflammatory mediators in serum were detected on Day 3 after treatment. Results The mechanical ventilation time and hospital stays in intensive care unit [(9.52 ± 1.41) vs. (14.57 ± 2.51) days] of patients in experimental group were significantly shorter than those in control group, and the number of cases developed into acute respiratory distress syndrome [1 (4.17%) vs. 9 (37.50%)] and multiple organ dysfunction syndrome [1 (4.17%) vs. 7 (29.17%)] was significantly less than those in control group. Oxygenation indexes (294.52 ± 41.26 vs. 257.63 ± 38.52; 357.74 ± 47.74 vs. 279.87 ± 31.46; 396.71 ± 55.12 vs. 279.87 ± 31.46) of patients were respectively calculated on Days 1, 2 and 3 after treatment, which were significantly higher than those in the control group. On Day 3 after treatment, the contents of serum C-reactive protein [(7.94 ± 1.05) vs. (14.49 ± 2.97) mg/L], tumor necrosis factor α [(264.69 ± 41.58) vs. (417.87 ± 64.51) ng/L], interleukin-6 (IL-6) [(147.72 ± 21.36) vs. (257.68 ± 41.54) ng/L], IL-8 [(93.68 ± 12.52) vs. (145.62 ± 22.65) ng/L], IL-10 [(205.64 ± 31.56) vs. (336.62 ± 51.38) ng/L] and myeloid cells-1 (73.32 ± 10.39 vs. 114.45 ± 18.51) of patients in experimental group were significantly lower than those in the control group. Conclusions The anisodamine combining with conventional therapy can relieve the degree of lung injury caused by acute pulmonary contusion, improve ventilatory function, lower the incidence of acute respiratory distress syndrome and multiple organ dysfunction syndrome and inhibit the activation of inflammatory reaction and the release of inflammatory mediators. [ABSTRACT FROM AUTHOR]

Purpose: To assess the effects of lipopolysaccharide (LPS) pretreatment on wound infection mouse model and evaluate the biological safety of the optimal pretreatment dose in vivo.Methods: Mice were pretreated with LPS of different doses at 48 and 24 h before femoral medial longitudinal incision was made and infected with different bacteria.Results: It is showed that 0.5 mg/kg/time of LPS pretreatment can significantly alleviate the inflammation in mouse model infected with methicillin-resistances Staphylococcus aureus, methicillin-sensitive S. aureus, Pseudomonas aeruginosa, or Escherichia coli compared with doses of 0.25 mg/kg/time, 1 mg/kg/time, and 1.5 mg/kg/time.Conclusions: LPS pretreatment can alleviate the inflammation in mouse model and the optimal dose is 0.5 mg/kg/time, and meanwhile it does not damage organs' function. [ABSTRACT FROM AUTHOR]

Objective To discuss the liver function damage mechanism of patients with clonorchiasis by analyzing the ultrasound characteristics, liver function, change of the serum inflammatory factors and cell apoptosis factors. Methods Color Doppler ultrasound technique was adopted to detect the portal vein and blood flow change of patients with clonorchiasis; ELISA was used to determine the level of different serum inflammatory factors. The levels of serum total bilirubin, serum albumin and glutamic-pyruvic transaminase were detected by automatic biochemical analyzer. Western blot was used to determine the expression of proteins relevant to apoptosis. Results Compared with the health control group, the trunk diameter of portal vein and the thickness of spleen, as well as the hepatic artery pulsation index of clonorchiasis patients increased obviously, the mean blood flow velocity of portal vein ( P < 0.05 or P < 0.01) decreased. The content of total bilirubin and transaminase in plasma increased significantly, but albumin decreased ( P < 0.05). Levels of TNF-α, IL-6 and IFN-γ increased remarkably, and the level of every factor was significantly different among patients with Child-Pugh , Child-Pugh II and Child-Pugh III classification of liver function ( P < 0.05 or P < 0.01). With the exacerbation of liver dysfunction, levels of TNF-α, IL-6 and IFN-γ gradually increased ( P < 0.05). Compared with the healthy control group, the expression quantity of apoptosis protein Fas, FasL, Bax and Caspase-3 increased significantly ( P < 0.05 or P < 0.01), but Bcl-2 decreased ( P < 0.05). Conclusions Changes of ultrasonic characteristics and liver dysfunction, caused by liver fluke infection, may be related to that both inflammatory response and apoptosis response have participated in the pathogenic process and liver damage course of clonorchiasis. [ABSTRACT FROM AUTHOR]

Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) 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.)

Summary The aim of this study was to evaluate the subcutaneous tissue reaction around zirconia-based materials. Forty-eight male Wistar Albino rats were used in this study. Disk-shaped (1 mm height and 5 mm diameter) samples composed of 67% spinel (MgAl 2 O 4 ), 27% tetragonal zirconia polycrystal, 4% (m/m) fly ash and 2% (m/m) boric acid were inserted into dorsal muscles of rats. After 1, 4, 8 and 16 weeks, the animals were sacrificed and zirconia materials were removed with the surrounding tissue. Tissue sections were made with a microtome and then stained with hematoxylin and eosin. Sections were evaluated for the intensity of inflammation. Additionally, the somatic and visceral lymph nodes were evaluated. Data were submitted to one-way analysis of variance (ANOVA) and Tukey HSD tests at a significant level of p < 0.05. There were statistically significant differences between mean inflammatory scores in different experimental periods ( p < 0.05). In addition, the inflammatory reaction decreased over time. The tested materials had no damaging effect on the rat lymph nodes and did not have a toxic action on the internal organs. Therefore, zirconia polycrystal tested in the present study may offer a promising treatment alternative after further mechanical and biological studies are performed. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Lung Cancer is the property of Chinese Journal of Lung Cancer 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.)

The article presents a study which examines the role of Buyang Huanwu Decoction fraction in attenuating inflammatory response and cellular apoptosis preventing cerebral ischemia/reperfusion injury. It is inferred that the Buyang Huanwu Decoction fraction contains saponins of Astragalus, safflower flavones and total paeony glycoside. The similarities in the effects between the Buyang Huanwu Decoction fraction and the Ginkgo biloba extract are highlighted.

Background & Aims: Celiac disease is a diet-induced, T cell–mediated enteropathy. The HLA variant DQ2.5 increases risk of the disease, and the homologous DQ2.2 confers a lower level of risk. As many as 5% of patients with celiac disease carry DQ2.2 without any other risk alleles. Epitopes commonly recognized by T cells of patients with HLA-DQ2.5 bind stably to DQ2.5 but unstably to DQ2.2. We investigated the response to gluten in patients with HLA-DQ2.2. Methods: We generated intestinal T-cell lines and clones from 7 patients with HLA-DQ2.2 (but not DQ2.5) and characterized the responses of the cells to gluten. The epitope off-rate was evaluated by gel filtration and T cell–based assays. Peptide binding to DQ2.2 was studied with peptide substitutes and DQ2 mutants. Results: Patients with DQ2.2 and no other risk alleles had gluten-reactive T cells that did not respond to the common DQ2.5-restricted T-cell epitopes. Instead, many of the T cells responded to a distinct epitope that was not recognized by those from patients with HLA-DQ2.5. This immunodominant epitope bound stably to DQ2.2. A serine residue at P3 was required for the stable binding. The effect of this residue related to a polymorphism at DQα22 that was previously shown to determine stable binding of peptides to DQ2.5. Conclusions: High levels of kinetic stability of peptide–major histocompatibility complexes are required to generate T-cell responses to gluten in celiac disease; the lower risk from DQ2.2 relates to constraints imposed on gluten peptides to stably bind this HLA molecule. These observations increase our understanding of the role of the major histocompatibility complex in determining T-cell responses in patients with celiac disease and are important for peptide-based vaccination strategies. [Copyright &y& Elsevier]

The Food and Drug Administration (FDA) indicates that bone morphogenetic protein (BMP) products are contraindicated in pediatric patients. However, it acknowledges the off-label use of BMP in difficult cases. Although the relative safety of BMP in children has been reported for lower extremity and spine procedures, little information exists for the safety of BMP used in the pediatric upper extremity. We present a case of a massive inflammatory reaction after use of recombinant human BMP-2 for repair of a symptomatic ulnar nonunion in a child. The case illustrates the potential difficulties of using the dose-dependent properties of BMP in the treatment of pediatric upper extremity nonunions when the dose calculations of BMP for children have not yet been defined. [ABSTRACT FROM AUTHOR]

The article discusses a study which evaluated the degree of adhesion formation and determined the uterine tissue malondialdehyde (MDA), nitric oxide (NO) and reduced glutathione (GSH) contents. The activities of catalase (CAT) and glutathione peroxidase (GPx) in an intraperitoneal adhesion model in adult rats receiving or not intraperitoneal installation of heparin or pentoxifylline were monitored. The results of the study showed that heparin and pentoxifylline can limit surgery-induced oxidative stress and regulate the inflammatory reaction, and heparin is more efficient than pentoxifylline in terms of preventing the intra-abdominal adhesion formation.

The objective of our study was to assess the influence of mechanical ventilation on healthy body organs. Fifteen piglets (aged 6 weeks, 19-27 kg) were anesthetized, instrumented, and divided into three groups: Group A - spontaneously breathing, group B - mechanically ventilated with tidal volume 6 ml/kg, and group C - ventilated with tidal volume 10 ml/kg for 12 hours. The parameters of lung, heart, liver and kidney functions neurohumoral regulation and systemic inflammatory reaction were recorded initially (time-1) and after 12 hours (time-12) of mechanical ventilation. At the onset of experiment (time-1) the levels of soluble adhesive molecules were higher (CAM; P<0.01), glomerular filtration index and free water clearance were lower (P<0.05) in both ventilated groups than in group A. Right ventricle myocardial performance index was higher (RIMP; P<0.05) in group C when compared with group A. Levels of CAM (P<0.05) and creatinine clearance (P<0.01) were higher, free water clearance was lower (P<0.05) in group C when compared to group B. At time-12 the RIMP (P<0.05) and levels of CAM were increased (P<0.01), creatinine clearance was decreased (P<0.05) in both ventilated groups compared to the same parameter at time-1. Ventilation index was higher (P<0.05), and hypoxemic index was lower (P<0.01) in group C when compared to group B. In conclusion, this study showed that mechanical ventilation induced changes compatible with early inflammatory response in healthy animals. Higher tidal volumes had detrimental effect on ventilatory parameters, reduced myocardial performance and potentiated adverse reaction of other organs. [ABSTRACT FROM AUTHOR]

Background: Alcoholic liver disease (ALD), one of the most prevalent forms of liver disease, has received wide attention worldwide. However, limited efficient and appropriate therapeutic agents were responded to ALD. Isoliquiritigenin (ISL), a flavonoid isolated from liquorice, possesses multiple pharmacological activities.Purpose: The current study investigated the hepatoprotective effect of ISL against ALD and further elucidate the involvement of miR-23a-3p/peroxisome proliferative activated receptor-γ coactivator 1 alpha (PGC-1α) in vivo and in vitro experiments.Study Design and Methods: In the study, H&E and Oil Red O staining were employed to detect liver histopathological changes and the accumulation of lipid droplets. Quantitative real-time PCR, bioinformatics, luciferase assay, immunofluorescence staining, reactive oxygen species (ROS), Western blot, and siRNA were used to further explore the mechanism of ISL protection.Results: ISL significantly reduced the liver-to-body weight ratios and biochemical index. The staining results showed that ISL remarkedly ameliorated the histopathological changes in the liver. Furthermore, ISL promoted fatty acid metabolism via induction in the expression of PGC-1α-target genes PPARα, CPT1α, and ACADs, and inhibited the ROS, TNF-α, IL-1β, and IL-6 expression. Bioinformatics and Luciferase assay analysis confirmed that miR-23a-3p might bind to PGC-1α mRNA in ALD. Significantly, the expression of miR-23a-3p was increased in the ALD, which was significantly decreased by ISL. In addition, the miR-23a-3p inhibitor also promoted lipid metabolism in ALD via PGC-1α activation.Conclusions: We first demonstrated that ISL could alleviate ALD, and further verified that ISL exerted protective effects through modulating miR-23a-3p/PGC-1α-mediated lipid metabolism in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Increasing evidence indicated that plaque stabilization is attributed to the composition of the atherosclerotic plaque, and inflammation plays an important role in the formation and progress of vulnerable atherosclerotic plaque (VAP), which is prone to rupture. Emodin, an important component of traditional Chinese herb rhubarb, has obvious anti-inflammatory effect, although its effect on atherosclerotic plaque stabilization is unknown. Apolipoprotein E (ApoE) is an important component of plasma lipoprotein with anti-atherosclerosis function, and the plaque in the aorta of ApoE-deficient mice has been demonstrated with characteristics of VAP. Therefore, this study was designed to determine whether emodin can stabilize the VAP in the ApoE-deficient mice and explain the possible mechanism. After fat-fed for 13 weeks, mice were randomized into three groups (11 animals/group) and intragastrically administrated with emodin, simvastatin or distilled water for 13 weeks, respectively. The plaque stability was evaluated by the morphology and composition of atherosclerotic plaques. Additionally, the expression of peroxisomal proliferator-activated receptor-γ (PPAR-γ), granulocyte-macrophage colony-stimulating factor (GM-CSF), and matrix metalloproteinase 9 (MMP-9) in plaques was determined by the immunohistochemistry method. We showed that emodin could decrease the lipid core area and the ratio of lipid to collagen content in plaques. In addition, emodin significantly inhibited the expression of GM-CSF and MMP-9, whereas it induced the expression of PPAR-γ in plaques. In conclusion, these results suggest that emodin can stabilize the VAP in the aortic root of ApoE-knockout mice, which is probably due to its anti-inflammatory effect. [ABSTRACT FROM AUTHOR]

Summary: We retrospectively reviewed the clinicopathological features of a series of 68 renal AA amyloidosis observations collected between 1990 and 2005. The amyloidogenic disease was a chronic infection (40.8%), a chronic inflammation (38%), a tumor (9.9%), a hereditary disease (9.9%), or was undetermined in 1.4% of cases. Nephrotic syndrome and renal insufficiency were noted in 63.1% and 75% of patients, respectively. The distribution pattern of glomerular amyloid deposits was mesangial segmental (14.7%), mesangial nodular (26.5%), mesangiocapillary (32.3%), and hilar (26.5%). Glomerular form was observed in 80.9% of cases and vascular form in 19.1%. AA amyloidosis-related inflammation was noted in 30 patients (44.1%) and appeared as a multinucleated giant cell reaction (27.9%) or a glomerular inflammatory infiltrate (25%), including glomerular crescents (17.6%). At the end of follow-up, 26 patients (38.2%) showed end-stage renal disease. The clinical presentation of glomerular and vascular forms was distinct with a clear predominance of proteinuria in glomerular form. Inflammatory reaction was preferentially observed in biopsies with a codeposition of immunoglobulin chains and/or complement factors in AA amyloid deposits. The distribution pattern of glomerular amyloid deposits and glomerular inflammatory reaction were independent factors influencing proteinuria level. Tubular atrophy, abundance, and distribution pattern of glomerular amyloid deposits at the time of biopsy were independent predictors of renal outcome. In conclusion, the glomerular involvement appeared as the determining histological factor for clinical manifestations and outcome of renal AA amyloidosis. AA amyloidosis-related inflammation could partly result from an immune response directed against AA fibrils and could induce amyloid resolution and crescents. [Copyright &y& Elsevier]

Studies revealed that particulate matter 2.5 (PM2.5) enters the lung through the respiratory tract and can damage lung tissue resulting in lung injury primarily via imbalance between pro-inflammatory and anti-inflammatory responses. Moreover, TLR4/NF-κB signaling pathways are reported to play a role in PM2.5-induced inflammation and lung injury, which is closely related to the inflammatory responses. Therefore, the traditional herbal formula, Deng-Shi-Qing-Mai-Tang (DSQMT), has been applied to improve patients' clinical symptoms with lung injury induced by PM2.5. It can reduce inflammatory reactions in lung injury and relieve cough and phlegm. However, the underlying mechanism of DSQMT treatment is still exclusive. To clarify the preventive and therapeutic effects of DSQMT on PM2.5-induced lung injury and explore its underlying mechanism. PM2.5-induced lung injury rat model was established, and DSQMT was administered. First, PM2.5 was collected, and PM2.5 suspension was prepared. Then, a rat model with PM2.5-induced lung injury was established, and the effects of DSQMT were evaluated in vivo. Finally, the roles of DSQMT in inhibiting the TLR4/NF-κB signaling pathway were investigated in vitro using the NR8383 cell line via Western blot analysis, real-time PCR, electrophoretic mobility shift assay (EMSA), and immunofluorescence staining, respectively and analyzed. We found that DSQMT significantly attenuated pathological lung tissue damage and inflammatory responses in PM2.5-induced lung injury. We also found that after PM2.5 stimulation in vitro , DSQMT regulates the expression of TLR4, MyD88, IKK, IκB-α, NF-κB p65 in the TLR4/NF-κB signaling pathway. It also constrains activated NF-κB entry into the nucleus and further limits its binding to target DNA. In addition, we revealed that DSQMT down-regulated interleukin (IL)-1β, IL-6, IL-10, THF-α, NO, PGE 2 to reduce the inflammatory response. We demonstrated that DSQMT has preventive and therapeutic effects on PM2.5-induced lung injury by down-regulation of the TLR4/NF-κB signaling pathway. Therefore, the efficacy of traditional Chinese medicine (TCM) in PM2.5 lung injury can be taken into consideration and may be improved in the future through further researches. [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Studies revealed that particulate matter 2.5 (PM2.5) enters the lung through the respiratory tract and can damage lung tissue resulting in lung injury primarily via imbalance between pro-inflammatory and anti-inflammatory responses. Moreover, TLR4/NF-κB signaling pathways are reported to play a role in PM2.5-induced inflammation and lung injury, which is closely related to the inflammatory responses. Therefore, the traditional herbal formula, Deng-Shi-Qing-Mai-Tang (DSQMT), has been applied to improve patients' clinical symptoms with lung injury induced by PM2.5. It can reduce inflammatory reactions in lung injury and relieve cough and phlegm. However, the underlying mechanism of DSQMT treatment is still exclusive.Purpose: To clarify the preventive and therapeutic effects of DSQMT on PM2.5-induced lung injury and explore its underlying mechanism.Study Design: PM2.5-induced lung injury rat model was established, and DSQMT was administered.Methods: First, PM2.5 was collected, and PM2.5 suspension was prepared. Then, a rat model with PM2.5-induced lung injury was established, and the effects of DSQMT were evaluated in vivo. Finally, the roles of DSQMT in inhibiting the TLR4/NF-κB signaling pathway were investigated in vitro using the NR8383 cell line via Western blot analysis, real-time PCR, electrophoretic mobility shift assay (EMSA), and immunofluorescence staining, respectively and analyzed.Results: We found that DSQMT significantly attenuated pathological lung tissue damage and inflammatory responses in PM2.5-induced lung injury. We also found that after PM2.5 stimulation in vitro, DSQMT regulates the expression of TLR4, MyD88, IKK, IκB-α, NF-κB p65 in the TLR4/NF-κB signaling pathway. It also constrains activated NF-κB entry into the nucleus and further limits its binding to target DNA. In addition, we revealed that DSQMT down-regulated interleukin (IL)-1β, IL-6, IL-10, THF-α, NO, PGE2 to reduce the inflammatory response.Conclusion: We demonstrated that DSQMT has preventive and therapeutic effects on PM2.5-induced lung injury by down-regulation of the TLR4/NF-κB signaling pathway. Therefore, the efficacy of traditional Chinese medicine (TCM) in PM2.5 lung injury can be taken into consideration and may be improved in the future through further researches. [ABSTRACT FROM AUTHOR]

Backgroud: Schisandra chinensis, a traditional Chinese medicine for liver protection, can significantly improve liver fibrosis. However, it is still unclear which active components in Schisandra chinensis play an anti-fibrosis role.Purpose: The purpose of present study was to observe the anti-fibrosis effect of schisantherin A (SCA) on liver fibrosis and explore its underlying mechanism.Methods: The liver fibrosis model of mice was constructed by the progressive intraperitoneal injection of thioacetamide (TAA), and SCA (1, 2, and 4 mg/kg) was administered by gavage for 5 weeks. The biochemical indicators and inflammatory cytokines were measured, changes in the pathology of the mice liver were observed by hematoxylin & eosin (H&E) and Masson stainings for studying the anti-fibrosis effect of SCA. A hepatic stellate cell (HSCs) activation model induced by transforming growth factor-β1 (TGF-β1) was established, and the effect of SCA on the HSCs proliferation was observed by MTT assay. The expressions of target proteins related to transforming growth factor-β-activated kinase 1 (TAK1)/mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways were evaluated by western blotting, immunohistochemistry or immunofluorescence analysis, to explore the potential mechanism of SCA.Results: SCA could significantly ameliorate the pathological changes of liver tissue induced by TAA, and reduce the serum transaminase level, the hydroxyproline level and the expression of α-smooth muscle actin (α-SMA) and collagen 1A1 (COL1A1) proteins in the liver tissue. SCA could significantly lower the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in the serum and liver tissue, and down-regulate the expression of target proteins related to TAK1/MAPK and NF-κB pathways in the liver tissue. The in vitro studies demonstrated that SCA significantly inhibited the proliferation and activation of HCS-T6 cells induced by TGF-β1, decreased TNF-α and IL-6 levels, and inhibited the TAK1 activation induced by TGF-β1 and then the expression of MAPK and NF-κB signaling pathway-related proteins.Conclusion: Together, SCA can ameliorate the liver fibrosis induced by TAA and the HSC-T6 cell activation induced by TGF-β1 in mice, and its mechanism may be to inhibit the HSCs activation and inflammatory response by inhibiting TGF-β1 mediated TAK1/MAPK and signal pathways. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. 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.)

Plastics and synthetic materials are polluting the world's oceans. In this study we exposed juvenile mussels, Mytilus edulis , to glass reinforced plastic (GRP) dust, under laboratory conditions. The study ran for a period of 7 days, to test for the morphological and potential physiological impacts of GRP. Infrared spectroscopy has revealed that the GRP resin material is poly diallyl phthalate. In mussels, particulate glass and plastics were detected in the digestive tubules and gills, with a suite of inflammatory features observed in all examined organs. In parallel, we observed the effect of powdered GRP on swimming behaviour and survival of water fleas, Daphnia magna. Polymer particles and fibreglass adhered to the filament hairs on appendages, including the caudal spine, in exposed organisms. Most importantly, swimming impairment and sinking of the animals were recorded shortly after exposure. The potential implications for severe localized impact of GRP on aquatic environment are discussed. • Glass Reinforced Particles (GRP) fragments tend to concentrate nearshore and impact coastal ecosystems. • A common poly ester resin (Poly diallyl phthalate) is holding the fibreglass particles together. • GRP particles accumulate in the mussel digestive gland and stimulate inflammatory reactions. • GRP particles adhere to the exoskeleton of water fleas and severely impact their swimming capacities. [ABSTRACT FROM AUTHOR]

Background & Aims: Thymic stromal lymphopoietin (TSLP) is a cytokine produced by epithelial cells that acts on dendritic cells, mast cells, T cells, and B cells. TSLP is involved in the pathogenesis of allergic inflammation in the lung and skin, but data indicate a regulatory role in the gastrointestinal tract. We tested the functional role of TSLP in mouse models of gastrointestinal allergy and tolerance. Methods: TSLP Receptor (TSLPR) +/+ and TSLPR−/− mice were sensitized and challenged with ovalbumin; models of allergic diarrhea or systemic anaphylaxis were studied. To induce oral tolerance, mice were fed with low-dose ovalbumin before they were immunized with it. Tolerance was measured from inhibition of ear swelling in a delayed-type hypersensitivity reaction. Results: TSLPR−/− mice were protected from the onset of allergic diarrhea; they did not develop mastocytosis in the jejunum and had reduced ovalbumin-immunoglobulin E in their serum, compared with TSLPR+/+ mice. TSLPR−/− mice also lost T helper cell (Th) 2-mediated inflammation in the jejunum. In contrast, sensitization and oral tolerance were not impaired in TSLPR−/− mice. Transfer of wild-type, Th2-primed cells to TSLPR−/− mice completely restored the development of allergic diarrhea. Antigen presentation assays showed that TSLPR on T cells, but not dendritic cells, was required to mediate the Th2 response. Conclusions: TSLP is required for allergic inflammation but not primary sensitization or tolerance to food proteins in the gastrointestinal tract; it amplifies Th2 responses directly from CD4+ T cells. [ABSTRACT FROM AUTHOR]