黄芪多糖通过抑制NF-κB和JNK信号通路减轻LPS诱导的小鼠心肌细胞凋亡

黄芪多糖通过抑制NF-κB和JNK信号通路减轻LPS诱导的
小鼠心肌细胞凋亡
韩琳;王洪新;鲁美丽
【期刊名称】《中国药理学通报》
【年(卷),期】2018(34)2
【摘要】Aim To study the effect of Astragalus polysaccharide (APS) on the apoptosis of cardiomyocytes induced by lipopolysaccharide (LPS) in mice and to explore its mechanism.Methods Kunming mice were treated with APS for 14 days,and intraperitoneal injection of LPS (10 mg · kg-1) was performed to establish cardiomyocyte apoptosis model in vivo,and H9c2 cells were pre-administered with APS.After 30 min,LPS (1 mg · L-1) was incubated for 24 hours to establish a model of cardiomyocyte apoptosis.Cardiac ejection fraction (EF) and left ventricular shortening score (FS) were measured using echocardiography in mice.TUNEL was carried to measure myocardial cell apoptosis.Enzyme-linked immunosorbent assay (ELISA) was employed to measure serum levels of IL-1β,TNF-α.Western blot was used to detect the expression of JNK,NF-κB signaling pathway and Bcl-2 family and caspase-3 protein in vivo and in vitro.Results LPS could significantly inhibit the left ventricular systolic function in mice and promote myocardial cell apoptosis.The levels of IL-
1β,TNF-α in serum,JNK,p-JNK,Bax,caspase-3 and the concentration of NF-κB in nucleus were all increased,while the level of Bcl-2 and the
concentration of NF-κB,IκB-α in cytoplasm were reduced.APS could significantly inhibit left ventricular systolic weakening in LPS-induced mice and cut down the apoptosis of cardiomyocytes.The secretion of IL-1β,TNF-α decreased to varying degrees.The protein level s of p-JNK,Bax,caspase-3 in myocardium and NF-κB in nucleus were down-regulated,but those of Bcl-2 and NF-κB,IκB-α in cytoplasm were up-regulated,and JNK had no significant change in vivo and in vitro.Conclusion APS ameliorates the LPS-induced apoptosis of myocardial cells by inhibiting NF-κB and JNK signaling pathway in mice.%目的研究黄芪多糖(Astragalus polysaccharide,APS)对脂多糖(lipopolysaccharide,LPS)诱导的小鼠心肌细胞凋亡的影响,并探讨其作用机制.方法体外实验采用H9c2细胞预先给予APS,30 min 后加入LPS(1 mg· L-1)共孵育24 h,建立心肌细胞凋亡模型.体内实验采用SPF级昆明小鼠预防性给予APS 14 d后,腹腔注射LPS (10mg·kg-1)建立心肌细胞凋亡模型.8h后采用超声心动测定小鼠心脏射血分数(EF)、左心室缩短分数(FS)
等;TUNEL测心肌细胞凋亡;ELISA检测血清中IL-1β、TNF-α含量;Western blot 检测组织和体外心肌细胞中JNK、NF-κB信号通路及Bcl-2家族、caspase-3相关蛋白表达.结果 LPS能明显抑制小鼠的左心室收缩功能;促使心肌细胞凋亡;增加血清中IL-1β、TNF-α,心肌细胞中JNK、p-JNK、Bax、caspase-3,胞核中NF-κB 蛋白浓度;降低Bcl-2和胞质中NF-κB、IκB-α蛋白浓度.APS能明显保护LPS诱导的小鼠心肌收缩功能,减少心肌细胞凋亡;减少血清中IL-1β、TNF-α,心肌组织细胞中p-JNK、Bax、caspase-3和胞核NF-κB蛋白含量;相对增加Bcl-2和胞质中NF-κB、IκB-α蛋白含量.而JNK蛋白表达无明显变化.结论 APS通过抑制NF-κB 和JNK信号通路,减轻LPS诱导的小鼠心肌细胞凋亡.
【总页数】7页(P243-249)
【作者】韩琳;王洪新;鲁美丽
【作者单位】锦州医科大学心脑血管药物研究重点实验室,辽宁锦州 121001;锦州医科大学心脑血管药物研究重点实验室,辽宁锦州 121001;锦州医科大学心脑血管药物研究重点实验室,辽宁锦州 121001
【正文语种】中文
【中图分类】R-332;R284.1;R332.11;R329.25;R392.12
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