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作 者:成永霞[1] 张大伟[2] 孙立新[1] 冯玉宽[1] 郭素芬[1] 刘贵波[2]
机构地区:[1]牡丹江医学院病理学教研室,牡丹江157011 [2]牡丹江医学院解剖教研室,牡丹江157011
出 处:《陕西医学杂志》2017年第7期819-822,共4页Shaanxi Medical Journal
基 金:国家青年基金资助项目(81500629)
摘 要:目的:观察GW3965对高糖诱导的心肌细胞凋亡的影响,并初步探讨其作用机制。方法:取对数期H9c2心肌细胞,随机分为对照组(Control组)、高糖诱导组(高糖组)和高糖诱导+激动剂处理组(GW3965组)。GW3965组细胞加入10μmol/L GW3965预处理24h,之后高糖组和GW3965组细胞加入33mmol/L葡萄糖继续诱导培养24h。采用MTT法检测细胞存活率,流式细胞术检测细胞凋亡率,JC-1荧光染料法检测线粒体膜电位,Western blot检测LXRα、ERK和p38 MAPK信号通路相关蛋白的变化。结果:GW3965可以提高H9c2抑制细胞凋亡,提高细胞存活率,改善细胞线粒体膜电位变化,并抑制ERK和p38 MAPK通路活性。结论:GW3965通过介导LXRα和MAPK通路减轻高糖诱导的细胞凋亡和线粒体损伤,对心肌细胞具有保护作用。Objective: To explore the effect of GW3965 on myocardial apoptosis induced by high glucose and its mechanism.Methods: H9c2 myocardial cells were randomly divided into three groups: control group, high glucose group and GW3965 group.Cells in GW3965 group were pretreated with 10μmol/L GW3965 for 24 h.Then cultures in high glucose group and GW3965 group were induced by 33 mmol/L glucose for 24 h.MTT was used to detect cells survival.The apoptosis was detected by flow cytometry and mitochondrial membrane potential by JC-1 fluorescence staining.Western blot was used to detect the expression of proteins related to LXR, ERK and p38 MAPK signal pathway.Results: GW3965 could inhibit the apoptosis of H9c2 cells, increase the rate of cells survival and influence mitochondrial membrane potential.GW3965 inhibited the activity of ERK and p38 MAPK pathway.Conclusion: GW3965 can inhibit the apoptosis and mitochondrial damage induced by high glucose via regulating LXRα and MAPK pathway, resulting a protective effect on myocardial cells.
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