段佳林,奚苗苗,牟 菲,蔺 瑞,赵美娜,卫 国,文爱东,张恩户.紫铆花素通过调节AMPK/GSK-3β信号通路抑制心肌缺血再灌注损伤[J].现代生物医学进展英文版,2017,17(14):2616-2621. |
紫铆花素通过调节AMPK/GSK-3β信号通路抑制心肌缺血再灌注损伤 |
Protective Effects and Possible Mechanism of Butein on Myocardial Ischemia Reperfusion Injury |
Received:December 06, 2016 Revised:January 03, 2017 |
DOI:10.13241/j.cnki.pmb.2017.14.004 |
中文关键词: 紫铆花素 心肌缺血再灌注 AMPK GSK-3β |
英文关键词: Butein Myocardial Ischemia/reperfusion Injury AMPK GSK-3β |
基金项目:国家自然科学基金面上项目(81470174);西京医院学科助推项目(XJZT15M19) |
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中文摘要: |
摘要 目的:研究紫铆花素对心肌缺血再灌注损伤的保护作用及其机制。方法:体外建立H9c2心肌细胞缺血再灌注模型,分为正常组、模型组、紫铆花素低、中和高剂量组(10,20 和40μM)。检测细胞存活率,LDH释放水平,试剂盒检测MDA、SOD、IL-1和IL-6水平,蛋白印迹法检测Bax,Bcl-2蛋白的表达以及AMPK和GSK-3β磷酸化水平。结果:与模型组比较,紫铆花素能够提高细胞存活率,减少LDH水平,降低MDA、IL-1和IL-6,增加SOD水平。减少Bax,Caspase-3蛋白的表达,增加 Bcl-2 蛋白的表达,提高 Bcl-2/Bax的比值(P <0.05)。同时,紫铆花素能够剂量依赖性的促进AMPK和GSK-3β磷酸化。进一步研究发现,紫铆花素的保护作用以及对GSK-3β的促磷酸化被AMPK抑制剂Compound C抵消。结论:紫铆花素能减轻心肌缺血再灌注损伤,抑制心肌细胞凋亡,其作用机制可能通过激活AMPK/GSK-3β信号通路,减轻氧化应激水平有关。 |
英文摘要: |
ABSTRACT Objective: To investigate the protective effects and possible mechanism of butein on myocardial ischemia/reperfusion injury. Methods: H9c2 cells were divided into normal control group, model group, low-dose, medium-dose and high-dose butein groups (10, 20 and 40 μM). After the drug was administered to cells for 24h, the myocardial ischemia-reperfusion injury was established. Cell viability, LDH, MDA, SOD, IL-1 and IL-6 were tested. The protein expressions of AMPK, Bax, Bcl-2, and GSK-3β were assayed by western blotting. Results: Comparedwith model group, butein could improve the cell survival rate, reduce the release of LDH, decrease the levels of MDA, IL-1 and IL-6, increase the level of SOD, decrease the expression of Bax, Caspase-3, increase the expression of Bcl-2and the ratio of Bcl-2 /Bax (P <0.05). In further study, we found that these protective effects were abolished by Compound C. Conclusion: Butein has the protective effects on myocardial ischemia/reperfusion injury in vitro, which can inhibit the myocardial injury through activating AMPK/ GSK-3β pathway. |
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