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Semaphorin 7A impairs barrier function in cultured human corneal epithelial cells in a manner dependent on nuclear factor-kappa b

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International Journal of Ophthalmology(English edition) 2024年第3期17卷 444-453页

作者： Cheng-Cheng Yang Xiu-Xia Yang Xiao-Jing Zhao Heng Wang Zi-Han Guo Kai Jin Yang Liu bin-Hui Li Department of Ophthalmology the Fifth Affiliated HospitalSun Yat-sen UniversityZhuhai 519000Guangdong ProvinceChina Department of Ophthalmology Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical UniversityHangzhou 310006Zhejiang ProvinceChina Eye Institute of Xiamen University Fujian Provincial Key Laboratory of Ophthalmology and Visual ScienceSchool of MedicineXiamen UniversityXiamen 361005Fujian ProvinceChina

●AIM:To evaluate the role of semaphorin 7A(Sema7A)and its associated regulatory mechanisms in modulating the barrier function of cultured human corneal epithelial cells(HCEs).●METHODS:barrier models of HCEs were treated with recombinant human Sema7A at concentrations of 0,125,250,or 500 ng/mL for 24,48,or 72h in *** electrical resistance(TEER)as well as Dextran-fluorescein isothiocyanate(FITC)permeability assays were conducted to assess barrier *** quantify tight junctions(TJs)such as occludin and zonula occludens-1(ZO-1)at the mRNA level,reverse transcriptionpolymerase chain reaction(RT-PCR)analysis was *** was used to examine the activity of the nuclear factor-kappa b(NF-κb)signaling pathway and the production of TJs *** analyses were employed to localize the ***-linked immunosorbent assay(ELISA)and RT-PCR were utilized to observe changes in interleukin(IL)-1β*** investigate the role of NF-κb signaling activation and IL^(-1)βin Sema7A’s anti-barrier mechanism,we employed 0.1μmol/L Iκb kinase 2(IKK2)inhibitor IV or 500 ng/mL IL^(-1)receptor(IL-1R)antagonist.●RESULTS:Treatment with Sema7A resulted in decreased TEER and increased permeability of Dextran-FITC in HCEs through down-regulating mRNA and protein levels of TJs in a time-and dose-dependent manner,as well as altering the localization of ***,Sema7A stimulated the activation of inhibitor of kappa b alpha(Iκbα)and expression of IL-1β.The anti-barrier function of Sema7A was significantly suppressed by treatment with IKK2 inhibitor IV or IL-1R antagonists.●CONCLUSION:Sema7A disrupts barrier function through its influence on NF-κb-mediated expression of TJ proteins,as well as the expression of IL-1β.These findings suggest that Sema7A could be a potential therapeutic target for the diseases in corneal epithelium.

关键词： human corneal epithelial barrier function transepithelial electrical resistance zonula occludens-1 occludin nuclear factor-kappa b

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Effects of Five Chitosan Oligosaccharides on nuclear factor-kappa b Signaling Pathway

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Journal of Wuhan University of Technology(Materials Science) 2012年第2期27卷 276-279页

作者：李贤周长忍 Department of Materials Science and Engineering Jinan University

The effects of five chito-oligomers, from dimer to hexamer （chitobiose, chitotriose, chitotetraose, chitopentaose, chitohexaose） separated from chitosan oligosaccharides, on nuclear factor -kappab （NF-rd3） signaling pathway were investigated by using luciferase assay and laser scanning microscopy. The expression of NF-rd3 downstream genes （cyclin DI, TNFa and IL-6） were tested by real time PCR. We found that all five chitosan oligosaccharides increased NF-Kb-dependent luciferase gene expression and NF-Kb downstream genes transcription, and the most significant were chitotetraose and chitohexaose. In addition, laser scanning microscopy experiments showed that chitotetraose and chitohexaose also activated the p65 subunite of NF-kb translocating from cytoplasm to nucleus, which suggested that they were the most potent activators of NF-kb signaling pathway.

关键词： chitosan chitosan oligosaccharide nuclear factor-kappa b inflammatory response

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Dietary saturated fatty acid and polyunsaturated fatty acid oppositely affect hepatic NOD-like receptor protein 3 inflammasome through regulating nuclear factor-kappa b activation

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World Journal of Gastroenterology 2016年第8期22卷 2533-2544页

作者： Yong-heng Sui Wen-jing Luo Qin-Yu Xu jing hua Division of Gastroenterology and Hepatology Ren Ji Hospital School of Medicine Shanghai Jiao Tong University Shanghai Institute of Digestive Disease

AIM: To investigate the effect of different dietary fatty acids on hepatic inflammasome ***: Wild-type C57bL/6 mice were fed either a high-fat diet or polyunsaturated fatty acid (PUFA)-enriched diet. Primary hepatocytes were treated with either saturated fatty acids (SFAs) or PUFAs as well as combined with lipopolysaccharide (LPS). The expression of NOD-like receptor protein 3 (NLRP3) inflammasome, peroxisome proliferator-activated receptor-γ and nuclear factor-kappa b (NF-κb) was determined by real-time PCR and Western blot. The activity of Caspase-1 and interleukine-1β production were ***: High-fat diet-induced hepatic steatosis was sufficient to induce and activate hepatic NLRP3 inflammasome. SFA palmitic acid (PA) directly activated NLRP3 inflammasome and increased sensitization to LPS-induced inflammasome activation in hepatocytes. In contrast, PUFA docosahexaenoic acid (DHA) had the potential to inhibit NLRP3 inflammasome expression in hepatocytes and partly abolished LPS-induced NLRP3 inflammasome activation. Furthermore, a high-fat diet increased but PUFA-enriched diet decreased sensitization to LPS-induced hepatic NLRP3 inflammasome activation in vivo. Moreover, PA increased but DHA decreased phosphorylated NF-κb p65 protein expression in ***: Hepatic NLRP3 inflammasome activation played an important role in the development of non-alcoholic fatty liver disease. Dietary SFAs and PUFAs oppositely regulated the activity of NLRP3 inflammasome through direct activation or inhibition of NF-κb.

关键词： Non-alcoholic fatty liver disease NOD-like receptor protein 3 inflammasome Saturated fatty acids Polyunsaturated fatty acids nuclear factor-kappa b

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Urinary trypsin inhibitor attenuates hepatic ischemia-reperfusion injury by reducing nuclear factor-kappa b activation

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Hepatobiliary & Pancreatic Diseases International 2009年第1期8卷 53-58页

作者： Wu, Yi-Jun Ling, Qi Zhou, Xin-Hui Wang, Yan Xie, Hai-Yang Yu, Ji-Ren Zheng, Shu-Sen Zhejiang Univ Sch Med Affiliated Hosp 1 Dept Gen Surg Hangzhou 310003 Zhejiang Peoples R China Zhejiang Univ Sch Med Affiliated Hosp 1 Dept Gynecol Hangzhou 310003 Zhejiang Peoples R China

bACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa b (NF-kappa b) and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines. We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS: Treatment group 1 (UTI given 5 minutes prior to liver ischemia), treatment group 2 (UTI given 5 minutes after the anhepatic phase) and a control group were investigated. blood and liver samples were obtained and compared at 1, 3, 6 and 24 hours after reperfusion. RESULTS: Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group (P kappa b activation. Also downregulated was the expression of tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory protein-2 at the mRNA level. P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated. In addition, the treatment group I showed a better protective effect against I/R injury than the treatment group 2. CONCLUSIONS: UTI reduces NF-kappa b activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury. The protective role of UTI is more effective in prevention than in treatment.

关键词： ischemia-reperfusion injury nuclear factor-kappa b tumor necrosis factor-alpha urinary trypsin inhibitor

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Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa b activation pathway in rats

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Hepatobiliary & Pancreatic Diseases International 2010年第2期9卷 169-174页

作者： Dong, Zhi-Zhen Yao, Deng-Fu Wu, Wei Yao, Min Yu, Hong-bo Shen, Jun-Jun Qiu, Li-Wei Yao, Ning-Hua Sai, Wen-Li Yang, Jun-Ling Nantong Univ Affiliated Hosp Res Ctr Clin Med Nantong 226001 Peoples R China Nantong Univ Affiliated Hosp Dept Diagnost Coll Med Nantong 226001 Peoples R China Nantong Univ Affiliated Hosp Dept Lab Med Nantong 226001 Peoples R China Nantong Univ Affiliated Hosp Dept Oncol Nantong 226001 Peoples R China Nantong Canc Hosp Dept Chemotherapy Nantong 226007 Peoples R China

bACKGROUND: The active form of nuclear factor-kappa b (NF-kappa b) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignancies. We investigated the dynamic expression of NF-kappa b and its influences on the occurrence of HCC through antiangiogenic (thalidomide) intervention in NF-kappa b activation. METHODS : Hepatoma models were induced with 2-fluorenylacetamide (2-FAA, 0.05%) in male Sprague-Dawley rats, and thalidomide (100 mg/kg body weight) was administered intragastrically to intervene in NF-kappa b activation. The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining. NF-kappa b mRNA was amplified by RT-nested PCR. The alterations of NF-kappa b and vascular endothelial growth factor (VEGF) expression were analyzed by enzyme-linked immunosorbent assay, immunohistochemistry, and Western blotting. RESULTS: Rat hepatocytes showed denatured, precancerous, and cancerous stages in hepatocarcinogenesis, with an increasing tendency of hepatic NF-kappa b, NF-kappa b mRNA, and VEGF expression, and their values in the HCC group were higher than those in controls (Pkappa b (chi(2)=9.93, Pkappa b is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-kappa b and VEGF, and delays the occurrence of HCC. (Hepatobiliary Pancreat Dis Int 2010; 9: 169-174)

关键词： hepatocellular carcinoma nuclear factor-kappa b vascular endothelial growth factor intervention dynamic expression

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Tonglian Decoction(通莲汤)Arrests the Cell Cycle in S-phase by Targeting the nuclear factor-kappa b Signal Pathway in Esophageal Carcinoma Eca109 Cells

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Chinese Journal of Integrative Medicine 2016年第5期22卷 384-389页

作者：贾永森胡雪琴李继安 Andras Szasz Gabriella Hegyi 韩炳生 basic Section College of Chinese MedicineNorth China University of Science and TechnologyTangshanHebei Province 063000China Institute of Orthopaedics and Traumatology Zhejiang Chinese Medical UniversityHangzhou 310053China Oncotherm Innovation and Trade Ltd. Pecs 7322Hungary Acupuncture Rehabilitation Foundation Budapest 1085Hungary Traditional Chinese Medicine Hospital of Shenzhen ShenzhenGuangdong Province 518020China

Objective： To investigate the anti-tumor activity and molecular mechanism of Tonglian Decoction （通莲汤, TLD） on esophageal carcinoma Eca109 cells. Methods： Ecal09 cells were treated with TLD and its separated formulae, including the clearing-heat and detoxification formula （Q）, activating-blood and promoting-qi formula （H） and nourishing-yin and blood formula （Z）. Cell proliferation was measured using the 3-（4,5-dimethyl-2- thiazolyl）-2,5-diphenyl-2-H-tetrazolium bromide assay, cell morphology was observed using a microscope, the cell cycle was measured using flow cytometry and the activity of the nuclear factor-kappa b （NF- K b） signal pathway was detected by Western blot. Results： The half maximal inhibitory concentrations of TLD, Q and H were 386, 771 and 729 rag/L, respectively. TLD, Q and H significantly inhibited cell proliferation, with 69.43%, 60.84% and 61.90% of treated cells in the G1 phase of the cell cycle. The percentage of cells in S phase increased significantly after treatment with TLD, Q, and H compared with the control group （P〈0.05）, and TLD showed the strongest effect. Z had no influence on the cell cycle compared with the control group （P〉0.05）. Western blot detection indicated slight differences in the inhibition of the NF- K b pathway by the different formulae. TLD formula strongly inhibited IKK β, NF- K b, interleukin-6 and tumor necrosis factor-α expression compared with the control group. Conclusions： TLD inhibited Eca109 cell proliferation by arresting cells in S phase. The possible mechanism might be related to inhibiting the NF- K b transduction cascade. The combination of the herbs found in the three separate formulae, H, Q and Z, work synergistically in TLD to produce the inhibitory effects of TLD treatment on Eca109 proliferation.

关键词： esophageal carcinoma Eca109 cells Tonglian Decoction proliferation cell cycle nuclear factor-kappa b Chinese medicine

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Testosterone alleviates tumor necrosis factor-alpha-mediated tissue factor pathway inhibitor downregulation via suppression of nuclear factor-kappa b in endothelial cells

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Asian Journal of Andrology 2009年第2期11卷 266-271页

作者： Hong Jin Wen-bing Qiu Yi-Fang Mei Qin Zhang Dong-Ming Wang Yu-Guang Li Xue-Rui Tan The First Affiliated Hospital of Shantou University Medical College Shantou 515041China The First Affiliated Hospital of Harbin Medical University Harbin 150081China

We have observed earlier that testosterone at physiological concentrations can stimulate tissue factor pathway inhibitor(TFPI)gene expression through the androgen receptor in endothelial *** study further investigated the impact of testosterone on TFPI levels in response to inflammatory cytokine tumor necrosis factor-alpha(TNF-α).Cultured human umbilical vein endothelial cells were incubated in the presence or absence of testosterone or TNF-α.TFPI protein and mRNA levels were assessed by enzyme-linked immunosorbent assay and quantitative real-time reverse transcription polymerase chain *** study the cellular mechanism of testosterone’s action,nuclear factor-kappa b(NF-κb)translocation was confirmed by electrophoretic mobility shift *** found that after NF-κb was activated by TNF-α,TFPI protein levels declined significantly by 37.3%compared with controls(Pb DNA-binding activity was significantly suppressed by testosterone(Pbotic effects on TFPI expression during inflammation by downregulating NF-κb activity.

关键词： nuclear factor-kappa b testosterone tissue factor pathway inhibitor

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Toll-like receptor 4/nuclear factor-kappa b signaling detected in brain after early subarachnoid hemorrhage

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Chinese Medical Journal 2009年第13期122卷 1575-1581页

作者： MA Chun-xiao YIN Wei-ning CAI bo-wen WU Jian WANG Jun-yi HE Min SUN Hong DING Jun-li YOU Chao Department of Neurosurgery West China Hospital Sichuan University Chengdu Sichuan 610041 China Institute of Digestive Surgery Key Laboratory of Transplant Engineering and Immunology Ministry of Health West China Hospital Sichuan University Chengdu Sichuan 610041 China

background Inflammation and immunity play a vital role in the pathogenesis of early brain injury after subarachnoid hemorrhage （SAH）. nuclear factor-kappa b （NF-κb） regulates many genes essential for inflammation and immunity and is activated by toll-like receptor （TLR）. This study aimed to detect the expression of the toll-like receptor 4/nuclear factor-kappa b （TLR4/NF-κb） signaling in the rat brain after early SAH. Methods The rats were decapitated and their brains were removed at 0, 2, 4, 6, 12, 24 and 48 hours after a single injection of blood into the prechiasmatic cistern, mRNA expression of TLR4 was measured by Taqman real-time RT-PCR, and protein expression by immunohistochemistry and Western blotting. NF-κb activity and concentrations of tumor necrosis factor-alpha （TNF-α）, interleukin-lbeta （IL-1β） and interleukin-6 （IL-6） were measured by enzyme-linked immunosorbent assay （ELISA）. Results TaqMan real-time RT-PCR and Western blotting identified a biphasic change in TLR4 expression in both mRNA and protein： an initial peak （2-6 hours） and a sustained elevation （12-48 hours）. Immunohistochemical staining showed the inducible expression of TLR4-like immunoreactions predominantly in glial cells and vascular endothelium. A similar biphasic change in the activation of NF-κb subunit p65 as well as the production of NF-κb-regulated proinflammatory cytokines （TNF-α, IL-1β and IL-6） were detected by ELISA. Conclusions These data suggest that experimental SAH induces significant up-regulation of TLR4 expression and the NF-κb signaling in early brain injury. Activation of the TLR4/NF-κb signaling may regulate the inflammatory responses after SAH.

关键词： subarachnoid hemorrhage toll-like receptor 4 nuclear factor-kappa b inflammatory cytokine

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Resolvin D1 Protects Lipopolysaccharide-induced Acute Kidney Injury by Down-regulating nuclear factor-kappa b Signal and Inhibiting Apoptosis

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Chinese Medical Journal 2016年第9期129卷 1100-1107页

作者： Yu-Liang Zhao Ling Zhang Ying-Ying Yang Yi Tang Jiao-Jiao Zhou Yu-Ying Feng Tian-Lei Cui Fang Liu Ping Fu Division of Nephrology West China Hospital Sichuan University Chengdu Sichuan 610041 China West China Kidney Research Institute Sichuan University Chengdu Sichuan 610041 China

background： Resolvin D1 （RvD1） is a newly found anti-inflammatory bioactive compound derived from polyunsaturated fatty acids. The current study aimed to explore the protective effect of RvD1 on lipopolysaccharide （LPS）-induced acute kidney injury （AKI） and its possible mechanism. Methods： both in vivo and in vitro studies were conducted. Male bALb/c mice were randomly divided into control group （saline）, LPS group （LPS 5 mg/kg）, RvD1 group （RvD1 5 μg/kg ＋ LPS 5 mg/kg）, and blockage group （boc-MLP 5 gg/kg ＋ RvD1 5 gg/kg ＋ LPS 5 mg/kg）. boc-MLP is a RvD 1 receptor blocker. The mice were intraperitoneally injected with these drugs and recorded for general condition for 48 h, while the blood and kidneys were harvested at 2, 6, 12, 24, and 48 h time points, respectively （n = 6 in each group at each time point）. Human proximal tubule epithelial cells （HK-2） were randomly divided into control group （medium only）, LPS group （LPS 5 μg/ml）, RvD1 group （RvD1 10 ng/ml ＋ LPS 5 μg/ml）, and blockage group （boc-MLP 10 ng/ml ＋ RvD1 10 ng/ml ＋ LPS 5 μg/ml）. The cells were harvested for RNA at 2, 4, 6, 12, and 24 h time points, respectively （n = 6 in each group at each time point）. blood creatinine was tested by using an Abbott i-STAT portable blood gas analyzer. Tumor necrosis factor-α （TNF-α level was detected by EL1SA. Kidney pathology was observed under hematoxylin and eosin （HE） staining and transmission electron microscope （TEM）. We hired immune-histological staining, Western blotting, and fluorescence quantitative polymerase chain reaction to detect the expression of RvD1 receptor ALX, nuclear factor-kappa b （NF-Kb） signaling pathway as well as caspase-3. Kidney apoptosis was evaluated by TUNEL staining. Results： RvD 1 receptor ALX was detected on renal tubular epithelials. Kaplan-Meier analysis indicated that RvD 1 improved 48 h animal survival （80%） compared with LPS group （40%） and RvDI blockage group （60%）, while RvD1 also ameliorated kidney pathological injury in HE stain

关键词： Acute Kidney Injury Apoptosis Lipopolysaccharide nuclear factor-kappa b Resolvin D1

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Pioglitazone ameliorates nonalcoholic steatohepatitis by down-regulating hepatic nuclear factor-kappa b and cyclooxygenases-2 expression in rats

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Chinese Medical Journal 2012年第13期125卷 2316-2321页

作者： ZHAO Jia-sheng ZHU Feng-shang LIU Su YANG Chang-qing CHEN Xi-mei Department of Endocrinology Tongji Hospital Tongji University School of Medicine Shanghai 200065 China Department of Gastroenterology Tongji Hospital Tongji University School of Medicine Shanghai 200065 China Department of Gastroenterology Central Hospital of ZhabeiDistrict Shanghai 200070 China

background Pioglitazone is effective in nonalcoholic steatohepatitis （NASH）, but the mechanisms of action are not completely understood. This study was designed to investigate the effects of pioglitazone on hepatic nuclear factor-kappa b （NF-Kb） and cyclooxygenases-2 （COX-2） expression in NASH rats. Methods Thirty Sprague-Dawley male rats were randomly assigned to a control group （n=10）, NASH group （n=10）, and pioglitazone treatment group （n=10）. Liver tissues were processed for histology by hematoxylin ＆ eosin and Masson stained. Serum alanine aminotransferase （ALT）, cholesterol, triglyceride, fasting blood glucose （FbG）, fasting insulin （FINS） levels and biochemical parameters of antioxidant enzyme activities, tumor necrosis factor alpha （TNF-a）, prostaglandin E2 （PGE2） levels in serum and liver were measured. The mRNA and protein expression of peroxisome proliferator-activated receptor gamma （PPARy）, NF-Kb and COX-2 were determined by real-time polymerase chain reaction, Western blotting and immunohistochemistry. One-way analysis of variance （ANOVA） and Wilcoxon＇s signed-rank test was used for the statistical analysis. Results There were severe steatosis, moderate inflammatory cellular infiltration and fibrosis in NASH rats. After pioglitazone treatment, steatosis, inflammation and fibrosis were significantly improved compared with the NASH group （X2=20.40, P 〈0.001; X2=20.17, P 〈0.001; X2=13.98, P=0.002）. Serum ALT, cholesterol, triglyceride, FbG, FINS levels were significantly elevated in the NASH group （P 〈0.05）. In the NASH group, total anti-oxidation competence （T-AOC）, superoxide dismutase （SOD）, catalase （CAT）, glutathione peroxidase （GSH-PX） and malondialdehyde （MDA） levels in serum and liver were conspicuous disordered than those parameters in the control group. Meanwhile, TNF-a and PGE2 levels in serum and liver were significantly increased compared with the control group. Immunohistochemistry showed NF-Kb and COX-2 expression in liver was significantly

关键词： pioglitazone nonalcoholic steatohepatitis peroxisome proliferator-activated receptor gamma,"cyclooxygenases-2 nuclear factor-kappa b

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