[1]王玲,黄佳.五味子乙素调控Jak2/Stat3信号通路抑制心肌细胞氧化应激损伤[J].西部中医药,2020,33(02):11-13.[doi:10.12174/j.issn.1004-6852.2020.02.03]
 WANG Ling,HUANG Jia.Schisandrin B Regulating Jak2/Stat3 Signaling Pathway in the Inhibitionof Oxidative Stress Damage of Myocardial Cells[J].Western Journal of Traditional Chinese Medicine,2020,33(02):11-13.[doi:10.12174/j.issn.1004-6852.2020.02.03]
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五味子乙素调控Jak2/Stat3信号通路抑制心肌细胞氧化应激损伤
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《西部中医药》[ISSN:2096-9600/CN:62-1204/R]

卷:
33
期数:
2020年02期
页码:
11-13
栏目:
出版日期:
2020-02-15

文章信息/Info

Title:
Schisandrin B Regulating Jak2/Stat3 Signaling Pathway in the Inhibitionof Oxidative Stress Damage of Myocardial Cells
文章编号:
1004-6852(2020)02-0011-03
作者:
王玲黄佳
恩施土家族苗族自治州中心医院,湖北 恩施 445000
Author(s):
WANG Ling, HUANG Jia△
Enshi Tujia and Miao Autonomous Prefecture Central Hospital, Enshi 445000, China
关键词:
五味子乙素心肌细胞氧化应激信号通路
Keywords:
schisandrin B myocardial cell oxidative stress signaling pathway
分类号:
R542.2
DOI:
10.12174/j.issn.1004-6852.2020.02.03
文献标志码:
A
摘要:
目的:研究五味子乙素(schisandrin B)对过氧化氢(H2O2)诱导心肌H9c2细胞氧化应激损伤的保护作用,并对其作用机制进行初步探讨。方法:体外培养H9c2细胞并构建氧化应激损伤模型,将细胞分为正常对照组、H2O2诱导组、H2O2+低剂量(10 μg/mL)五味子乙素组、H2O2+中剂量(50 μg/mL)五味子乙素组、H2O2+高剂量(150 μg/mL)五味子乙素组,CCK-8试剂检测H9c2细胞增殖情况,相关试剂盒检测丙二醛(malonaldehyde,MDA)、一氧化氮(nitric oxide,NO)含量及超氧化物岐化酶(superoxide dismutase,SOD)活性,Western Blot检测细胞中Jak2、p-Jak2、Stat3、p-Stat3(Tyr705、Ser727)、血红素氧合酶1(oxygenase-1,HO-1)和超氧化物歧化酶(superoxide dismutase-1,SOD-1)蛋白表达水平。结果:与H2O2诱导组相比,低、中、高剂量五味子乙素组细胞相对存活率显著升高,细胞匀浆氧化应激产物MDA、NO水平显著降低、SOD-1酶活性显著升高,HO-1、SOD-1、p-Jak2及p-Stat3蛋白表达水平显著升高,差异比较均有统计学意义(P<0.05),并且均表现出剂量依赖性。结论:五味子乙素对H9c2细胞氧化应激损伤具有保护作用,其作用机制主要通过激活Jak2/Stat3信号通路来实现。
Abstract:
Objective: To study schisandrin B in the protection of hydrogen peroxide (H202)-induced oxidative stress damage in myocardial H9c2 cells, and initially explore its mechanism. Methods: H9c2 cells were cultured in vitro, prepared into the models with oxidative stress damage, and they were divided into normal control group, H202 - induced group, the groups of H202 + low dose (10 μg/mL) of schisandrin B, H202 + moderate dose (50 μg/mL) of schisandrin B, and H202 + high dose (150 μg/mL) of schisandrin B, CCK-8 reagent was used to measure H9c2 cellular proliferation, the related kit to detect the contents of MDA and NO, and the activity of SOD, Western blot to measure the expressions of Jak2, p-Jak2, Stat3, p-Stat3 (Tyr705, Ser727), HO-1 and SOD1 protein. Results: Compared with H202 - induced group, cellular relative survival rates of low, moderate and high doses groups of schisandrin B rose significantly, the levels of oxidative stress products MDA and NO in cell homogenate lowered signficantly, the activity of SOD1 enzyme rose notaly, the levels of HO-1, SOD-1, p - Jak2 and p - Stat3 protein lifted notably, and the difference showed statistical meaning (P<0.05), in the dose-dependent manner. Conclusion: Schisandrin B could protect oxidative stress damage in H9c2 cells, and its mechanism might be realized through the activation of Jak2/Stat3 signaling pathway.

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备注/Memo

备注/Memo:
收稿日期:2019-04-08作者简介:王玲(1985—),女,主治医师。研究方向:心血管疾病的防治。通讯作者:黄佳(1985—),女,副主任医师。研究方向:心血管疾病的防治。
更新日期/Last Update: 2020-02-15