19 results on '"Chen, Yan"'
Search Results
2. Decreased Vδ2 γδ T Cells Associated With Liver Damage by Regulation of Th17 Response in Patients With Chronic Hepatitis B
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Wu, Xiaoli, Zhang, Ji-Yuan, Huang, Ang, Li, Yuan-Yuan, Zhang, Song, Wei, Jun, Xia, Siyuan, Wan, Yajuan, Chen, Weiwei, Zhang, Zheng, Li, Yangguang, Wen, Ti, Chen, Yan, Tanaka, Yoshimasa, Cao, Youjia, Wang, Puyue, Zhao, Liqing, Wu, Zhenzhou, Wang, Fu-Sheng, and Yin, Zhinan
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- 2013
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3. Gancao Nourishing-Yin decoction combined with methotrexate in treatment of aging CIA mice: a study based on DIA proteomic analysis.
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Chen, Yong, Zhu, Xing-wang, Lai, Wing-Fu, Liu, Yong-pu, Xu, Xuan-feng, Liu, Li-ming, Chen, Yan-juan, Zhang, Chuan-fu, Wang, Guang-yi, Cheng, Zhi-qiang, and Liu, Dong-zhou
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BIOLOGICAL models ,CYTOKINES ,C-reactive protein ,BIOMARKERS ,HERBAL medicine ,COMBINATION drug therapy ,OSTEOCLASTS ,STAINS & staining (Microscopy) ,ANIMAL experimentation ,INFLAMMATION ,SERUM ,METABOLISM ,BLOOD collection ,PROTEOMICS ,METHOTREXATE ,SEVERITY of illness index ,CELLULAR signal transduction ,BIOINFORMATICS ,RHEUMATOID arthritis ,ENZYME-linked immunosorbent assay ,DRUG synergism ,GENOTYPES ,FACTOR analysis ,DESCRIPTIVE statistics ,MASS spectrometry ,RESEARCH funding ,FOLIC acid ,CLUSTER analysis (Statistics) ,DATA analysis software ,CHINESE medicine ,MICE ,PHENOTYPES ,PHARMACODYNAMICS - Abstract
Background: Elderly rheumatoid arthritis (ERA) population faces multiple treatment dilemma. Here we aim to investigate if Gancao Nourishing-Yin decoction (GCNY) added to methotrexate (MTX) exhibit better effects in an ERA mice model. Methods: ERA mice model was established by adding D-galactose (Dgal) to collagen-induced arthritis (CIA) mice. The model was then assigned into control group (CIA + Dgal), MTX treatment group (MTX), GCNY treatment group (GCNY), and integrative treatment group (MTX + GCNY). Pathological scoring was performed to evaluate the severity between the groups. Proteomic analysis was applied to investigate the secretory phenotype of the ERA mouse model and the underlying mechanism of GCNY, MTX and their combination. Representative cytokines related to proteomic results were further validated by ELISAs. Results: CIA + Dgal mice showed more aggressive joints damage than the CIA mice. Besides changes in the inflammatory pathway such as Pi3k-Akt signaling pathway in both model, differential expressed proteins (DEPs) indicated metabolism-related pathways were more obvious in CIA + Dgal mice. Low-dose MTX failed to show pathological improvement in CIA + Dgal mice, while GCNY improved joints damage significantly. Besides down-regulated inflammation-related targets, GCNY-regulated DEPs (such as Apoc1 ~ 3, Grk2 and Creb3l3) were broadly enriched in metabolism-related pathways. MTX + GCNY showed the best therapeutic effect, and the DEPs enriched in a variety of inflammatory,metabolism and osteoclast differentiation signaling pathway. Notably, MTX + GCNY treatment up-regulated Dhfr, Cbr1, Shmt1 involved in folic acid biosynthesis and anti-folate resistance pathways indicated a coincidence synergic action. ELISAs confirmed CPR and Akt that elevated in CIA + Dgal mice were significantly ameliorated by treatments, and adding on GCNY elevated folic acid levels and its regulator Dhfr. Conclusion: Aging aggravated joints damage in CIA, which probably due to metabolic changes rather than more severe inflammation. GCNY showed significant effects in the ERA mice model especially when integrated with MTX to obtain a synergic action. [ABSTRACT FROM AUTHOR]
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- 2023
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4. Lactate Is a Key Mediator That Links Obesity to Insulin Resistance via Modulating Cytokine Production From Adipose Tissue.
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Lin, Yijun, Bai, Meijuan, Wang, Shuo, Chen, Lingling, Li, Zixuan, Li, Chenchen, Cao, Peijuan, and Chen, Yan
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CYTOKINES ,OBESITY ,RESEARCH ,INFLAMMATION ,ANIMAL experimentation ,RESEARCH methodology ,ANIMAL nutrition ,EVALUATION research ,COMPARATIVE studies ,INSULIN resistance ,LACTIC acid ,ADIPOSE tissues ,MICE - Abstract
Numerous evidence indicates that inflammation in adipose tissue is the primary cause of systemic insulin resistance induced by obesity. Obesity-associated changes in circulating LPS level and hypoxia/HIF-1α activation have been proposed to be involved in boosting obesity-induced inflammation. However, there is poor understanding of what triggers obesity-induced inflammation. In this study, we pinpoint lactate as a key trigger to mediate obesity-induced inflammation and systemic insulin resistance. Specific deletion of Slc16a1 that encodes MCT1, the primary lactate transporter in adipose tissues, robustly elevates blood levels of proinflammatory cytokines and aggravates systemic insulin resistance without alteration of adiposity in mice fed high-fat diet. Slc16a1 deletion in adipocytes elevates intracellular lactate level while reducing circulating lactate concentration. Mechanistically, lactate retention due to Slc16a1 deletion initiates adipocyte apoptosis and cytokine release. The locally recruited macrophages amplify the inflammation by release of proinflammatory cytokines to the circulation, leading to insulin resistance in peripheral tissues. This study, therefore, indicates that lactate within adipocytes has a key biological function linking obesity to insulin resistance, and harnessing lactate in adipocytes can be a promising strategy to break this link. [ABSTRACT FROM AUTHOR]
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- 2022
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5. Vinpocetine Inhibits NF-κB-Dependent Inflammation in Acute Ischemic Stroke Patients
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Chen Yan, Fu-Dong Shi, Junwei Hao, Xiaofeng Ma, Yang Yao, Fang Zhang, Dawei Zang, Shoufeng Liu, Zhongying Gong, Changjuan Wei, and Jieli Chen
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Adult ,Male ,0301 basic medicine ,medicine.medical_specialty ,Magnetic Resonance Spectroscopy ,Time Factors ,Neurology ,Inflammation ,Pharmacology ,Statistics, Nonparametric ,Brain Ischemia ,Brain ischemia ,Pathogenesis ,03 medical and health sciences ,Cerebral circulation ,0302 clinical medicine ,Vinpocetine ,Humans ,Medicine ,RNA, Messenger ,Vinca Alkaloids ,Aged ,biology ,business.industry ,General Neuroscience ,C-reactive protein ,NF-kappa B ,Middle Aged ,medicine.disease ,Magnetic Resonance Imaging ,Stroke ,IκBα ,C-Reactive Protein ,Neuroprotective Agents ,030104 developmental biology ,Gene Expression Regulation ,Anesthesia ,Leukocytes, Mononuclear ,biology.protein ,Cytokines ,Female ,Neurology (clinical) ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,030217 neurology & neurosurgery ,Follow-Up Studies ,medicine.drug - Abstract
Immunity and inflammation play critical roles in the pathogenesis of acute ischemic stroke. Therefore, immune intervention, as a new therapeutic strategy, is worthy of exploration. Here, we tested the inflammation modulator, vinpocetine, for its effect on the outcomes of stroke. For this multi-center study, we recruited 60 patients with anterior cerebral circulation occlusion and onset of stroke that had exceeded 4.5 h but lasted less than 48 h. These patients, after random division into two groups, received either standard management alone (controls) or standard management plus vinpocetine (30 mg per day intravenously for 14 consecutive days, Gedeon Richter Plc., Hungary). Vinpocetine treatment did not change the lymphocyte count; however, nuclear factor kappa-light-chain-enhancer of activated B cell activation was inhibited as seen not only by the increased transcription of IκBα mRNA but also by the impeded phosphorylation and degradation of IκBα and subsequent induction of pro-inflammatory mediators. These effects led to significantly reduced secondary lesion enlargement and an attenuated inflammation reaction. Compared to controls, patients treated with vinpocetine had a better recovery of neurological function and improved clinical outcomes during the acute phase and at 3-month follow-up. These findings identify vinpocetine as an inflammation modulator that could improve clinical outcomes after acute ischemic stroke. This study also indicated the important role of immunity and inflammation in the pathogenesis of acute ischemic stroke and the significance of immunomodulatory treatment. Clinical Trial Registration Information: www.clinicaltrials.gov . Identifier: NCT02878772
- Published
- 2017
6. Regulation of hypothalamic-pituitary-adrenal axis activity and immunologic function contributed to the anti-inflammatory effect of acupuncture in the OVA-induced murine asthma model
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Jingcheng Dong, Yubao Lv, Chen Yan, Ying Wei, Feng Liu, Ming Dong, Jing Sun, Qingli Luo, Ling Zhong, Shuming Mo, Jiaqi Liu, and Fei Xu
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0301 basic medicine ,Eotaxin ,Cortisol secretion ,Hypothalamo-Hypophyseal System ,medicine.medical_specialty ,Ovalbumin ,medicine.drug_class ,Acupuncture Therapy ,Pituitary-Adrenal System ,Adrenocorticotropic hormone ,Anti-inflammatory ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Acupuncture ,Animals ,Medicine ,Asthma ,Inflammation ,Mice, Inbred BALB C ,Tumor Necrosis Factor-alpha ,business.industry ,General Neuroscience ,respiratory system ,Eosinophil ,medicine.disease ,respiratory tract diseases ,Disease Models, Animal ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,Immunology ,Cytokines ,Female ,business ,030217 neurology & neurosurgery ,Hypothalamic–pituitary–adrenal axis - Abstract
Asthma is a complex inflammatory disease of the airways and acupuncture is one of the effective therapies widely used to treat asthma in China. The aim of the study was to evaluate the regulatory role of acupuncture in airway inflammation and the hypothalamic-pituitary-adrenal (HPA) axis activity in OVA-induced murine asthma model. Our results demonstrated that acupuncture was effective in suppression of AHR, inhibition of total leukocyte, neutrophil, lymphocyte and eosinophil counts in BALF, attenuation of airway inflammation and TNF-α, IL-1β, IL-5 and eotaxin secretion. Furthermore, the HPA axis activity was also regulated by acupuncture, which included promotion of adrenocorticotropic hormone and cortisol secretion in the plasma. Our findings revealed that acupuncture could attenuate airway inflammation and regulate HPA axis and immunologic function in the OVA-induced murine asthma model, which may provide support to better understand the contribution of acupuncture to the regulation of airway inflammation and HPA axis activity in asthma.
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- 2017
7. Stromal cell-derived factor-1 regulates the secretion of interleukin-1β in the temporomandibular joint of rats with synovial inflammation.
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Qi, Dong, Sun, Shuzhen, Han, Liang, Wang, Qiang, Kong, Jingjing, Zhang, Yujun, Wang, Ronglin, Chen, Yan, and Ji, Ping
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SYNOVITIS ,TEMPOROMANDIBULAR disorders ,INTERLEUKIN-1 ,CELLULAR signal transduction ,STROMAL cells ,SECRETION ,CYTOKINES ,TEMPOROMANDIBULAR joint ,SYNOVIAL membranes ,INFLAMMATION ,RATS ,RESEARCH funding ,CONNECTIVE tissue cells ,ANIMALS - Abstract
Background: Synovitis is characterized by the infiltration of inflammatory cells and often accompanies the pathological progression of the clinical symptoms affecting the temporomandibular joint (TMJ), such as pain, snapping, and limited mouth opening. It has been suggested that the signal transduction pathway and resultant proinflammatory mediators play important roles in the pathogenesis of synovitis. Therefore, in this present research, we aimed to investigate the changes in the expressions of stromal cell-derived factor 1 (SDF-1) and interleukin (IL)-1β in rats with occlusal interference.Materials and Methods: We divided 36 male Wistar rats into the following groups: Group A (control group), Group B (occlusal interference group), and Group C (AMD3100 group). Synovial inflammation was induced in the rats in Groups B and C to establish the occlusal interference model. The inflammatory changes were detected, and the expressions of SDF-1 and IL-1β in the synovium were assayed via immunostaining and a real-time quantitative polymerase chain reaction (PCR).Results: In Group B, obvious inflammatory changes were observed in the synovial membranes; additionally, the SDF-1 and IL-1β expression levels were significantly higher at the protein and mRNA levels. However, in Group C, these experimental results were inhibited by an injection with AMD3100.Conclusion: These results may indicate that SDF-1 regulates the expression level of inflammatory factors, such as IL-1β, in the synovial membranes of rats with occlusal interference. Our findings suggest that the SDF-1 axis may contribute to the onset of synovitis during the development of TMJ joint disease. [ABSTRACT FROM AUTHOR]- Published
- 2020
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8. A20 down-regulation promotes UVB-induced inflammation via activation of the NF-κB pathway.
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Chen, Yan, Wu, Wenjuan, Li, Xing, Guo, Yanni, Lu, Fengyan, Man, Maoqiang, Jin, Yumei, Yang, Chunyan, Chai, Yanjie, and He, Li
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SKIN inflammation , *INFLAMMATION , *SECRETION , *CYTOKINES , *SKIN - Abstract
• A20 expression was decreased in CAD skin tissues and in UVB- irradiated HaCaT cells. • Secretion of cytokines showed similar trends in CAD skin lesions and in UVB irradiated cells. • A20 knock-down or over-expression altered secretion of inflammatory cytokines through the NF-κB pathway. • Since UVB-induced inflammation is associated with A20, which could provide new insight into the discussion of skin inflammation related to CAD. [ABSTRACT FROM AUTHOR]
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- 2020
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9. The role of pro-inflammatory cytokines in lipid metabolism of metabolic diseases.
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Chen, Yan, Yu, Chun-Yan, and Deng, Wei-Min
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LIPID metabolism , *METABOLIC disorders , *LIPID synthesis , *CYTOKINES , *BLOOD lipids , *INFLAMMATION , *CANCER , *ATHEROSCLEROSIS , *FATTY liver - Abstract
Adipose tissue has been considered as a crucial source of certain pro-inflammatory cytokines; conversely, these pro-inflammatory cytokines are involved in regulating the proliferation and apoptosis of adipocytes, promoting lipolysis, inhibiting lipid synthesis and decreasing blood lipids, etc. In recent decades, extensive studies have indicated that pro-inflammatory cytokines play important roles in the development of lipid metabolism of metabolic diseases, including obesity, atherosclerosis, steatohepatitis and hyperlipoproteinemia. However, the involved pro-inflammatory cytokines types and the underlying mechanisms remain largely unknown. The "re-discovery" of cancer as a metabolic disorder largely occurred in the last five years. Although pro-inflammatory cytokines have been intensively investigated in cancer research, there are very few studies about the roles of pro-inflammatory cytokines in the lipid metabolism of cancer. In the current review, we provide an overview of the progress that has been made in the roles of different pro-inflammatory cytokines in lipid metabolism of metabolic diseases including cancer. [ABSTRACT FROM AUTHOR]
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- 2019
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10. CFTR Deletion in Mouse Testis Induces VDAC1 Mediated Inflammatory Pathway Critical for Spermatogenesis
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Xie Jiang, Sun Huaqin, Xu Wenming, Liao Huijuan, Chen Yan, Qin Lang, and Yang Ming
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0301 basic medicine ,Male ,Physiology ,lcsh:Medicine ,Cystic Fibrosis Transmembrane Conductance Regulator ,RNA-binding proteins ,Cystic fibrosis ,Biochemistry ,Heat Shock Response ,Epithelium ,Reproductive Physiology ,Animal Cells ,Immune Physiology ,Testis ,Medicine and Health Sciences ,Cell Cycle and Cell Division ,lcsh:Science ,Energy-Producing Organelles ,Cellular Stress Responses ,Regulation of gene expression ,Innate Immune System ,Multidisciplinary ,Chromosome Biology ,NF-kappa B ,respiratory system ,Sertoli cell ,Cell biology ,Mitochondria ,Meiosis ,medicine.anatomical_structure ,Cell Processes ,Cytokines ,Signal transduction ,Cellular Types ,Anatomy ,Cellular Structures and Organelles ,VDAC1 ,Germ cell ,Research Article ,Signal Transduction ,medicine.medical_specialty ,congenital, hereditary, and neonatal diseases and abnormalities ,Immunology ,Biology ,Bioenergetics ,Research and Analysis Methods ,03 medical and health sciences ,Internal medicine ,medicine ,Animals ,Mice, Inbred CFTR ,Heat shock ,Spermatogenesis ,Immunohistochemistry Techniques ,Inflammation ,Sertoli Cells ,Endoplasmic reticulum ,Voltage-Dependent Anion Channel 1 ,lcsh:R ,Biology and Life Sciences ,Proteins ,Epithelial Cells ,Cell Biology ,Molecular Development ,medicine.disease ,Histochemistry and Cytochemistry Techniques ,030104 developmental biology ,Endocrinology ,Germ Cells ,Biological Tissue ,Gene Expression Regulation ,Immune System ,Immunologic Techniques ,lcsh:Q ,Gene Deletion ,Developmental Biology - Abstract
Cystic fibrosis is the most common genetic disease among Caucasians and affects tissues including lung, pancreas and reproductive tracts. It has been shown that Endoplasmic Reticulum (ER) stress and heat shock response are two major deregulated functional modules related to CFTR dysfunction. To identify the impact of CFTR deletion during spermatogenesis, we examined the expression of spermiogenesis-related genes in the testis of CFTR mutant mice (CF mice). We confirmed expression changes of MSY2, a germ cell specific RNA binding protein, resulting from deletion of CFTR in testis. Furthermore, real time PCR and Western blot results showed that an inflammatory response was activated in CF mice testis, as reflected by the altered expression of cytokines. We demonstrate for the first time that expression of MSY2 is decreased in CF mice. Our results suggest that CFTR deletion in testis influences inflammatory responses and these features are likely to be due to the unique environment of the seminiferous tubule during the spermatogenesis process. The current study also suggests avenues to understand the pathophysiology of CFTR during spermatogenesis and provides targets for the possible treatment of CFTR-related infertility.
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- 2016
11. Tetrahydrocurcumin, a major metabolite of curcumin, ameliorates allergic airway inflammation by attenuating Th2 response and suppressing the IL‐4Rα‐Jak1‐STAT6 and Jagged1/Jagged2 ‐Notch1/Notch2 pathways in asthmatic mice.
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Chen, Bin Lin, Chen, Yan Qiu, Ma, Bai Hui, Yu, Si Fei, Li, Li Yue, Zeng, Qing Xiang, Zhou, Yu Tao, Wu, Yin Fan, Liu, Wen long, Wan, Jian Bo, Yang, Yan, and Li, Chun Wei
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METABOLITES , *CURCUMIN , *INFLAMMATION , *ASTHMA , *CYTOKINES - Abstract
Summary: Background: Curcumin (Cur), derived from Curcuma species, exhibits anti‐inflammatory, antioxidant, and anticancer effects. Although Cur has some beneficial effects on asthma, its clinical application is limited by its low bioavailability. Tetrahydrocurcumin (THC), the major active metabolite of Cur, has multiple biological functions, similarly to Cur, and importantly, it showed enhanced bioavailability in tissues and plasma. However, the effect of THC on asthma has not been reported. Objective: The current study sought to investigate the efficacy of dietary THC on allergic asthma compared to that of Cur in an animal model. Methods: The anti‐inflammatory effects of Cur and THC were evaluated in an ovalbumin‐induced asthmatic mouse model. The nasal symptoms, pathological alterations of the lung tissues, oxidants and antioxidants, cytokine production, T cell subsets, and Th2‐related signalling pathway activity were assessed. Results: Both THC and Cur had beneficial effects on asthmatic mice with regard to nasal symptoms, pathological changes (eosinophils and mucus hyper‐production), oxidative stress (malondialdehyde), cytokine production (IL‐13), Th17 and cytotoxic T cell subsets, and Th2 signalling pathway (IL‐4Rα‐Jak1‐STAT6 and Jagged1/Jagged2‐Notch1/Notch2 axis) activity. THC was more effective than Cur in suppressing tissue eosinophilia, mucus production, and IL‐4Rα/Jak1/STAT6 pathway activity. Furthermore, only THC inhibited peripheral eosinophil levels, Th2 cytokines (IL‐4 and IL‐5), and Th2 cell subsets and enhanced an antioxidant enzyme (glutathione). Conclusion and Clinical Relevance: The above results demonstrated for the first time that THC was superior to Cur in modulating allergic asthmatic phenotypes, especially attenuating the Th2 response. THC might be a potentially effective agent for asthma treatment. [ABSTRACT FROM AUTHOR]
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- 2018
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12. The mechanism of action of safflower total flavonoids in the treatment of endometritis caused by incomplete abortion based on network pharmacology and 16S rDNA sequencing.
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Chen, Yan, Xiang, Qiwen, Peng, Fu, Gao, Song, Yu, Lei, Tang, Yunli, Yang, Zhou, Pu, Wei, Xie, Xiaofang, and Peng, Cheng
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DNA analysis , *HEMORRHAGE prevention , *CYTOKINES , *INTERLEUKINS , *MEDICINAL plants , *FLAVONOIDS , *ENDOMETRIAL diseases , *SEQUENCE analysis , *ANIMAL experimentation , *INFLAMMATION , *IMMUNOHISTOCHEMISTRY , *WESTERN immunoblotting , *ONCOGENES , *PHOSPHOTRANSFERASES , *GUT microbiome , *RATS , *CELLULAR signal transduction , *UTERUS , *JANUS kinases , *FORECASTING , *TUMOR necrosis factors , *INCOMPLETE miscarriage , *PHARMACEUTICAL chemistry , *COMPUTER-assisted molecular modeling , *MITOGEN-activated protein kinases , *NITRIC oxide , *CASPASES , *DISEASE risk factors , *DISEASE complications - Abstract
Safflower is a traditional Chinese medicine used for treating gynaecological diseases. However, its material basis and mechanism of action in the treatment of endometritis induced by incomplete abortion are still unclear. This study aimed to reveal the material basis and mechanism of action of safflower in the treatment of endometritis induced by incomplete abortion through comprehensive methods, including network pharmacology and 16S rDNA sequencing. Network pharmacology and molecular docking methods were used to screen the main active components and potential mechanisms of action of safflower in the treatment of endometritis induced by incomplete abortion in rats. A rat model of endometrial inflammation by incomplete abortion was established. The rats were treated with safflower total flavonoids (STF) based on forecasting results, serum levels of inflammatory cytokines were analysed, and immunohistochemistry, Western blots, and 16S rDNA sequencing were performed to investigate the effects of the active ingredient and the treatment mechanism. The network pharmacology prediction results showed 20 active components with 260 targets in safflower, 1007 targets related to endometritis caused by incomplete abortion, and 114 drug-disease intersecting targets, including TNF, IL6, TP53, AKT1, JUN, VEGFA, CASP3 and other core targets, PI3K/AKT, MAPK and other signalling pathways may be closely related to incomplete abortion leading to endometritis. The animal experiment results showed that STF could significantly repair uterine damage and reduce the amount of bleeding. Compared with the model group, STF significantly down-regulated the levels of pro-inflammatory factors (IL-6, IL-1β, NO, TNF-α) and the expression of JNK, ASK1, Bax, caspase3, and caspase11 proteins. At the same time, the levels of anti-inflammatory factors (TGF-β and PGE2) and the protein expression of ERα, PI3K, AKT, and Bcl2 were up-regulated. Significant differences in the intestinal flora were seen between the normal group and the model group, and the intestinal flora of the rats was closer to the normal group after the administration of STF. The characteristics of STF used in the treatment of endometritis induced by incomplete abortion were multi-targeted and involved multiple pathways. The mechanism may be related to the activation of the ERα/PI3K/AKT signalling pathway by regulating the composition and ratio of the gut microbiota. [Display omitted] [ABSTRACT FROM AUTHOR]
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- 2023
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13. Remote ischemic preconditioning STAT3-dependently ameliorates pulmonary ischemia/reperfusion injury.
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Luo, Nanfu, Liu, Jin, Chen, Yan, Li, Huan, Hu, Zhaoyang, and Abbott, Geoffrey W.
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LUNG transplantation ,STAT proteins ,ISCHEMIA ,REPERFUSION injury ,CYTOKINES - Abstract
The lungs are highly susceptible to injury, including ischemia/reperfusion (I/R) injury. Pulmonary I/R injury can occur when correcting conditions such as primary pulmonary hypertension, and is also relatively common after lung transplantation or other cardiothoracic surgery. Methods to reduce pulmonary I/R injury are urgently needed to improve outcomes following procedures such as lung transplantation. Remote liver ischemic preconditioning (RLIPC) is an effective cardioprotective measure, reducing damage caused by subsequent cardiac I/R injury, but little is known about its potential role in pulmonary protection. Here, we analyzed the efficacy and mechanistic basis of RLIPC in a rat model of pulmonary I/R injury. RLIPC reduced lung I/R injury, lessening structural damage, inflammatory cytokine production and apoptosis. In addition, RLIPC preserved pulmonary function compared to controls following lung I/R injury. RLIPC stimulated phosphorylation of pulmonary STAT3, a component of the SAFE signaling pathway, but not phosphorylation of RISK pathway signaling proteins. Accordingly, STAT3 inhibition using AG490 eliminated the pulmonary protection afforded by RLIPC. Our data demonstrate for the first time that RLIPC protects against pulmonary I/R injury, via a signaling pathway requiring STAT3 phosphorylation. [ABSTRACT FROM AUTHOR]
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- 2018
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14. Translocation of Endogenous Danger Signal HMGB1 From Nucleus to Membrane Microvesicles in Macrophages.
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Chen, Yan, Li, Guangping, Liu, Yanxia, Werth, Victoria P., Williams, Kevin Jon, and Liu, Ming ‐ Lin
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NUCLEAR proteins , *CYTOKINES , *INFLAMMATION , *CELL membranes , *SMOKING , *MACROPHAGES - Abstract
High mobility group box 1 (HMGB1) is a nuclear protein that can be released from activated or dead cells. Extracellular HMGB1 can serve as a 'danger signal' and novel cytokine that mediates sterile inflammation. In addition to its soluble form, extracellular HMGB1 can also be carried by membrane microvesicles. However, the cellular mechanisms responsible for nuclear HMGB1 translocation to the plasma membrane and release onto membrane microvesicles have not been investigated. Tobacco smoking is a major cause of sterile inflammation in many diseases. Smoking also increases blood levels of HMGB1. In this study, we found that exposure of macrophages to tobacco smoke extract (TSE) stimulated HMGB1 expression, redistribution, and release into the extracellular milieu both as a soluble molecule and, surprisingly, as a microvesicle-associated form (TSE-MV). Inhibition of chromosome region maintenance-1 (CRM1), a nuclear exporter, attenuated TSE-induced HMGB1 redistribution from the nucleus to the cytoplasm, and then its release on TSE-MVs. Our study demonstrates a novel mechanism for the translocation of nuclear HMGB1 to the plasma membrane, and then its release in a microvesicle-associated form. J. Cell. Physiol. 231: 2319-2326, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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15. Impeding the interaction between Nur77 and p38 reduces LPS-induced inflammation.
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Li, Li, Liu, Yuan, Chen, Hang-zi, Li, Feng-wei, Wu, Jian-feng, Zhang, Hong-kui, He, Jian-ping, Xing, Yong-zhen, Chen, Yan, Wang, Wei-jia, Tian, Xu-yang, Li, An-zhong, Zhang, Qian, Huang, Pei-qiang, Han, Jiahuai, Lin, Tianwei, and Wu, Qiao
- Subjects
INFLAMMATION ,NERVE growth factor ,LIPOPOLYSACCHARIDES ,CYTOKINES ,NF-kappa B ,MITOGEN-activated protein kinases - Abstract
Sepsis, a hyperinflammatory response that can result in multiple organ dysfunctions, is a leading cause of mortality from infection. Here, we show that orphan nuclear receptor Nur77 (also known as TR3) can enhance resistance to lipopolysaccharide (LPS)-induced sepsis in mice by inhibiting NF-κB activity and suppressing aberrant cytokine production. Nur77 directly associates with p65 to block its binding to the κB element. However, this function of Nur77 is countered by the LPS-activated p38α phosphorylation of Nur77. Dampening the interaction between Nur77 and p38α would favor Nur77 suppression of the hyperinflammatory response. A compound, n-pentyl 2-[3,5-dihydroxy-2-(1-nonanoyl) phenyl]acetate, screened from a Nur77-biased library, blocked the Nur77-p38α interaction by targeting the ligand-binding domain of Nur77 and restored the suppression of the hyperinflammatory response through Nur77 inhibition of NF-κB. This study associates the nuclear receptor with immune homeostasis and implicates a new therapeutic strategy to treat hyperinflammatory responses by targeting a p38α substrate to modulate p38α-regulated functions. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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16. ω-3 fatty acids suppress inflammatory cytokine production by macrophages and hepatocytes.
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Hao, Wei, Wong, Olive Y., Liu, Xuelai, Lee, Puiyan, Chen, Yan, and Wong, Kenneth K.Y.
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OMEGA-3 fatty acids ,CYTOKINES ,IMMUNOSUPPRESSION ,MACROPHAGES ,LIVER cells ,TOTAL parenteral feeding ,LIVER diseases ,LIVER failure - Abstract
Abstract: Objective: Long-term total parenteral nutrition (TPN) in children is often complicated by parental nutrition–associated liver disease and may even lead to liver failure. Recently, the addition of ω-3 fatty acids to TPN has been shown to reduce the risk of parental nutrition–associated liver disease. The purpose of this study was to explore the anti-inflammatory effects of ω-3 fatty acids (eicosapentaenoic acid [EPA]) to demonstrate the protection of the liver against hepatic steatosis and damage. Materials and Methods: Lipopolysaccharide (LPS) and prostaglandin E
2 (PGE2 ) were used to stimulate human macrophages and hepatocytes (THLE-3) to induce in vitro inflammatory condition. The cells were then incubated with either ω-3 (EPA) or ω-6 (arachidonic acid) fatty acids. Supernatants were collected at different time points for the measurement of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and interleukin 10 (IL-10) using enzyme-linked immunosorbent assay. Furthermore, pretreated macrophages by LPS stimulation and after incubation with EPA were added to prestimulated hepatocytes for the subsequent measurement of cytokine response. Results: Eicosapentaenoic acid effectively reduced LPS-induced or PGE2 -induced TNF-α and IL-6 expression, and increased IL-10 expression significantly when compared with arachidonic acid. Furthermore, supernatant collected after co-culturing EPA with macrophages also suppressed the levels of TNF-α and IL-6 in hepatocytes. This would suggest that EPA not only had an anti-inflammatory effect on macrophages and hepatocytes directly, it could indirectly reduce hepatocyte inflammation through activated macrophages. Conclusions: The addition of ω-3 fatty acids in TPN suppresses the inflammatory response via direct and indirect routes. The findings may help explain the clinical benefits of EPA in pediatric patients receiving long-term TPN. [Copyright &y& Elsevier]- Published
- 2010
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17. Momordica charantia (Bitter Melon) Reduces Obesity-Associated Macrophage and Mast Cell Infiltration as well as Inflammatory Cytokine Expression in Adipose Tissues.
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Bao, Bin, Chen, Yan-Guang, Zhang, Lei, Na Xu, Yan Lin, Wang, Xin, Liu, Jian, and Qu, Wei
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MOMORDICA charantia , *MACROPHAGES , *MAST cells , *ADIPOSE tissues , *CYTOKINES , *GENE expression , *INFLAMMATION - Abstract
Obesity is a world-wide epidemic disease that correlates closely with type 2 diabetes and cardiovascular diseases. Obesity-induced chronic adipose tissue inflammation is now considered as a critical contributor to the above complications. Momordica charantia (bitter melon, BM) is a traditional Chinese food and well known for its function of reducing body weight gain and insulin resistance. However, it is unclear whether BM could alleviate adipose tissue inflammation caused by obesity. In this study, C57BL/6 mice were fed high fat diet (HFD) with or without BM for 12 weeks. BM-contained diets ameliorated HFD-induced obesity and insulin resistance. Histological and real-time PCR analysis demonstrated BM not only reduced macrophage infiltration into epididymal adipose tissues (EAT) and brown adipose tissues (BAT). Flow cytometry show that BM could modify the M1/M2 phenotype ratio of macrophages in EAT. Further study showed that BM lowered mast cell recruitments in EAT, and depressed pro-inflammatory cytokine monocyte chemotactic protein-1 (MCP-1) expression in EAT and BAT as well as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expression in EAT. Finally, ELISA analysis showed BM-contained diets also normalized serum levels of the cytokines. In summary, in concert with ameliorated insulin resistance and fat deposition, BM reduced adipose tissue inflammation in diet-induced obese (DIO) mice. [ABSTRACT FROM AUTHOR]
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- 2013
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18. Isoforskolin pretreatment attenuates lipopolysaccharide-induced acute lung injury in animal models
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Yang, Weimin, Qiang, Dongjin, Zhang, Min, Ma, Limei, Zhang, Yonghui, Qing, Chen, Xu, Yunlong, Zhen, Chunlan, Liu, Jikai, and Chen, Yan-Hua
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FORSKOLIN , *ENDOTOXINS , *LUNG injury treatment , *ANIMAL models in research , *ARACHIDONIC acid , *CYTOKINES , *ADULT respiratory distress syndrome , *INTERLEUKINS - Abstract
Abstract: Isoforskolin was isolated from Coleus forskohlii native to Yunnan in China. We hypothesize that isoforskolin pretreatment attenuates acute lung injury induced by lipopolysaccharide (endotoxin). Three acute lung injury models were used: situ perfused rat lung, rat and mouse models of endotoxic shock. Additionally, lipopolysaccharide stimulated proinflammatory cytokine production was evaluated in human mononuclear leukocyte. In situ perfused rat lungs, pre-perfusion with isoforskolin (100, and 200μM) and dexamethasone (65μM, positive control) inhibited lipopolysaccharide (10 mg/L) induced increases in lung neutrophil adhesion rate, myeloperoxidase activity, lung weight Wet/Dry ratio, permeability-surface area product value, and tumor necrosis factor (TNF)-α levels. In rats, pretreatments with isoforskolin (5, 10, and 20 mg/kg, i.p.) and dexamethasone (5mg/kg, i.p.) markedly reduced lipopolysaccharide (6mg/kg i.v.) induced increases of karyocyte, neutrophil counts and protein content in bronchoalveolar lavage fluid, and plasma myeloperoxidase activity. Lung histopathology showed that morphologic changes induced by lipopolysaccharide were less pronounced in the isoforskolin and dexamethasone pretreated rats. In mice, 5 mg/kg isoforskolin and dexamethasone caused 100% and 80% survival, respectively, after administration of lipopolysaccharide (62.5mg/kg, i.v., 40% survival if untreated). In human mononuclear leukocyte, isoforskolin (50, 100, and 200μM) and dexamethasone (10μM) pre-incubation lowered lipopolysaccharide (2μg/mL) induced secretion of the cytokine TNF-α, and interleukins (IL)-1β, IL-6, and IL-8. In conclusion, pretreatment with isoforskolin attenuates lipopolysaccharide-induced acute lung injury in several models, and it is involved in down-regulation of inflammatory responses and proinflammatory cytokines TNF-α, IL-1β, IL-6, and IL-8. [Copyright &y& Elsevier]
- Published
- 2011
- Full Text
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19. Saponins from Nigella glandulifera seeds attenuate collagen-induced rheumatoid arthritis in rats via the OPG/RANKL/NF-κB and Ang/Tie-2 pathways.
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Jiang, Hailun, Xu, Fang, Zeng, Li, Li, Chenyang, Chen, Yan, Wang, Linlin, Li, Zhuorong, and Liu, Rui
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PHYTOTHERAPY , *COLLAGEN , *DRUG efficacy , *CYTOKINES , *INTERLEUKINS , *HIGH performance liquid chromatography , *SYNOVITIS , *ANIMAL experimentation , *CONVALESCENCE , *GROWTH factors , *GLYCOSIDES , *INTERLEUKIN-1 , *ANKLE , *CELLULAR signal transduction , *RATS , *QUALITATIVE research , *SEVERITY of illness index , *INTERFERONS , *SEEDS , *RHEUMATOID arthritis , *MASS spectrometry , *PATHOLOGIC neovascularization , *TUMOR necrosis factors , *DNA-binding proteins , *PLANT extracts , *VASCULAR endothelial growth factors , *T cells , *KNEE ,THERAPEUTIC use of plant extracts - Abstract
Nigella glandulifera Freyn et Sint. (N. glandulifera) seeds are widely used in traditional Uyghur medicine for a variety of immuno-inflammatory diseases. The total saponins from N. glandulifera seeds (TSNGS) have been shown to have analgesic, antioxidant, and anti-inflammatory effects that can alleviate joint pain and swelling. Rheumatoid arthritis (RA) is a chronic and progressive, debilitating autoimmune disease for which current treatments are not sufficiently effective and result in unsatisfactory side effects. This study aimed to mechanistically investigate the therapeutic effects of TSNGS on RA. Qualitative analysis of TSNGS was performed using ultra-high-performance liquid chromatography-Q-Orbitrap-high-resolution mass spectrometry. Rats with collagen-induced arthritis (CIA), IL-1β-induced HFLS-RAs, and VEGF-induced HUVECs were analyzed to determine the efficacy and mechanism of TSNGS on RA. Twenty-one compounds were identified in TSNGS. TSNGS (10, 50, or 250 mg/kg) reduced the severity of arthritis, indicated by a lower arthritis score, reduced paw swelling, and body weight in rats with CIA. TSNGS ameliorated histopathological changes involving inflammatory infiltration, bone degeneration, and angiogenesis in knee and ankle joints. TSNGS improved the immuno-inflammatory response by restoring the levels of the cytokines IFN-γ, TNF-α, IL-1β, IL-6, IL-17A, IL-4, and IL-10, and increasing the number of CD4+CD25+ Tregs in the peripheral circulation and Foxp3 levels in knee joints in rats with CIA. Furthermore, TSNGS increased the OPG/RANKL ratio and downregulated p-p65 in serum and joint synovia. Inhibition of angiogenesis by TSNGS was associated with recovery of the angiogenesis-related Ang/Tie-2 signaling pathway. It was established that TSNGS provides a therapeutic effect on RA by alleviating synovitis, bone degeneration, and angiogenesis via the OPG/RANKL/NF-κB and Ang/Tie-2 pathways and may be used for the treatment of RA. [Display omitted] • TSNGS may have potential as a novel treatment for RA. • TSNGS decreased the severity of arthritis in rats with CIA. • TSNGS reduced synovitis associated with RA via OPG/RANKL/NF-κB pathway. • TSNGS alleviated angiogenesis related to RA via Ang/Tie-2 signaling. • TSNGS upregulated the level of CD4+CD25+ Tregs and Foxp3 in rats with CIA. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
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