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作 者:张妍 田立群[1] 冯莹[1] 张盈盈 王代宗 易春峰 ZHANG Yan;TIAN Li-Qun;FENG Ying;ZHANG Ying-Ying;WANG Dai-Zong;YI Chun-Feng(Department of Cardiology,Wuhan No.1 Hospital,Wuhan 430022,China)
出 处:《中国免疫学杂志》2021年第8期927-930,共4页Chinese Journal of Immunology
基 金:武汉市卫计委项目(WX18D53)。
摘 要:目的:探讨抑制高迁移率族蛋白B1(HMGB1)对心肌梗死(MI)大鼠心肌纤维化的影响及机制。方法:15只雄性SD大鼠随机分为正常组、模型组、HMGB1抑制组,每组5只,结扎冠状动脉缺血30 min再灌注法构建MI模型,HE染色观察心肌组织病理变化,Masson染色观察心肌组织纤维化程度,Western blot检测Ⅰ型胶原蛋白(COL-Ⅰ)、基质金属蛋白酶2(MMP-2)、转化生长因子β1(TGF-β1)HMGB1、Toll样受体4(TLR4)、NF-κB及p-NF-κB表达。结果:与模型组相比,HMGB1抑制组大鼠心肌纤维化及炎症浸润缓解,心肌胶原纤维减少;Western blot结果显示,与对照组相比,模型组大鼠COL-Ⅰ、MMP-2、TGF-β1、HMGB1、TLR4、p-NF-κB蛋白表达显著提高(P<0.05),HMGB1抑制组蛋白表达情况逆转。结论:抑制HMGB1表达对MI引起的心肌纤维化具有一定抑制作用,其机制可能与调控TLR4/NF-κB信号通路有关。Objective:To investigate effect of high mobility group protein B1(HMGB1)inhibition on myocardial fibrosis induced by myocardial infarction(MI)in rats and its mechanism.Methods:15 male SD rats were randomly divided into normal group,model group and HMGB1 inhibition group,5 in each group.MI model was constructed by ligating coronary artery ischemia for30 min reperfusion.Pathological changes of myocardial tissue were observed by HE staining,and degree of fibrosis of myocardial tissue was observed by Masson staining.Expressions of Collagen I(COL-Ⅰ),matrix metalloproteinase 2(MMP-2)and transforming growth factorβ1(TGF-β1),HMGB1,TLR4,NF-κB and p-NF-κB were detected by Western blot.Results:Compared with model group,myocardial fibrosis and inflammatory infiltration in HMGB1 inhibition group were reduced,and myocardial collagen fibers were reduced.Western blot showed that,compared with control group,COL-Ⅰ,MMP-2,TGF-β1,HMGB1,TLR4,p-NF-κB protein expressions in model group were significantly increased(P<0.05).HMGB1 inhibition group could reverse these changes.Conclusion:Inhibition of HMGB1 expression can inhibit myocardial fibrosis caused by MI,whose mechanism may be related to regulation of TLR4/NF-κB signaling pathway.
关 键 词:高迁移率族蛋白B1 心肌梗死 心肌纤维化 TLR4/NF-κB信号通路
分 类 号:R542.22[医药卫生—心血管疾病]
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