摘要
目的探讨黄芪甲苷对H9c2心肌细胞缺氧/复氧损伤的保护作用及可能机制。方法将H9c2心肌细胞分为假手术组(Control),缺氧/复氧模型组(H/R)和AS-IV低(ASIVL)、高剂量(ASIVH)治疗组。CCK-8检测H9c2细胞活性;LDH检测H9c2细胞的损伤程度;流式细胞仪检测细胞凋亡;qRT-PCR和Western blot分别检测H9c2细胞GRP78、ATF-6、p-PERK mRNA和蛋白的表达。结果AS-IV可提高H9c2细胞缺氧复氧后的活性,减少LDH释放量,抑制细胞凋亡,缓解细胞损伤;同时进一步研究发现,AS-IV可以下调氧化应激相关蛋白GRP78、ATF-6、p-PERK的表达。结论AS-IV抑制缺氧/复氧损伤H9c2心肌细胞内质网应激、改善心肌细胞损伤与抑制PERK信号通路相关。
Objective To investigate the protective effect of Astragaloside IV(AS-IV)on hypoxia/reoxygenation(H/R)injury in H9 c2 cardiomyocytes and to explore its possible mechanism.Methods H9 c2 cardiomyocytes were divided into sham operation group(sham),hypoxia/reoxygenation model group(H/R)and AS-IV low(ASIVL)and high dose(ASIVH)treatment groups.CCK-8 was used to detect the activity of H9 c2 cells,;LDH was used to detect the damage of H9 c2 cells,flow cytometry was used to detect apoptosis,qRT-PCR and Western-blot were used to detect the expression of GRP78,ATF-6 and p-PERK mRNA and protein in H9 c2 cells,respectively.Results AS-IV increased the activity of H9 c2 cells after hypoxia-reoxygenation,reduced the release of LDH,inhibited cell apoptosis and alleviated cell damage,downregulated the expressions of oxidative stress-related proteins GRP78 and ATF-6 and p-PERK.Conclusion AS-IV inhibited the endoplasmic reticulum stress of H9 c2 cardiomyocytes induced by hypoxia/reoxygenation and alleviated myocardial cell injury,which is related to the inhibition of PERK signaling pathway.
作者
葛红吉
郭媛利
周南
于洋
GE Hong-ji;GUO Yuan-li;ZHOU Nan;YU Yang(Department of Circulatory and Internal Medicine,Tieling Central Hospital,Liaoning Province,Tie Ling 112001;Department of Anesthesiology,General Hospital of the Northern People’s Liberation Army,Shenyang 110016,China)
出处
《解剖科学进展》
2020年第5期514-517,521,共5页
Progress of Anatomical Sciences
基金
辽宁省自然科学基金(20180551091)。
作者简介
通信作者:葛红吉。
