和厚朴酚对高脂所致心肌细胞氧化应激损伤的保护作用及其与内质网应激-线粒体凋亡通路的相关性

The protective effect of honokiol on oxidative stress injury of cardiomyocytes induced by high fat and its relationship with endoplasmic reticulum stress-mitochondrial apoptosis pathway

目的探讨和厚朴酚对高脂所致心肌细胞氧化应激损伤的保护作用及其与内质网应激-线粒体凋亡通路的相关性。方法用棕榈酸(palmitic acid,PA)建立心肌细胞脂毒性损伤模型,和厚朴酚预处理1 h,MTT法评估心肌细胞增殖能力;用试剂盒检测心肌细胞氧化应激、凋亡及线粒体膜电位水平;Western blot法评估内质网应激-线粒体凋亡通路相关蛋白表达。结果PA(0.4 mmol·L-1)刺激24、48 h,可显著降低细胞增殖能力,成功建立心肌细胞脂毒性损伤模型,高脂刺激条件设置为PA(0.4 mmol·L-1)刺激24 h;另一方面,高脂可明显增加细胞内活性氧(reactive oxygen species,ROS)水平,降低线粒体膜电位水平,促进细胞凋亡,增加内质网应激-线粒体凋亡通路相关蛋白表达水平。和厚朴酚预处理1 h,可以明显逆转上述变化。结论和厚朴酚对高脂所致心肌细胞氧化应激损伤有明显的保护作用,其作用机制与内质网应激-线粒体凋亡通路相关。

Aim To investigate the protective effect of honokiol on oxidative stress injury of cardiac myocytes induced by high fat and its relationship with endoplasmic reticulum stress-mitochondrial apoptosis pathway.Methods The lipotoxic injury model of cardiomyocyte was established by palmitic acid(PA).The proliferation of cardiomyocyte was evaluated by MTT after pretreatment with honokiol.The levels of oxidative stress and apoptosis of cardiomyocyte were measured by kit.The expression of endoplasmic reticulum stress-mitochondrial apoptotic pathway-related protein was evaluated by Western blot.Results PA(0.4 mmol·L-1)stimulated for 24 and 48 h could significantly reduce the cell proliferation ability,and successfully establish a model of cardiacmyocyte lipid toxicity injury.The high-fat stimulation condition was set as PA(0.4 mmol·L-1)stimulated for 24 h.On the other hand,high fat could significantly increase intracellular reactive oxygen species(ROS)level and decrease mitochondrial membrane potential level and promote cell death.High fat can significantly increase the expression of endoplasmic reticulum stress-mitochondrial apoptotic pathway-related proteins.Pretreatment with honokiol could significantly reverse the above changes.Conclusions Honokiol has obvious protective effect on oxidative stress injury of cardiomyocytes induced by high fat,and its mechanism is related to endoplasmic reticulum stress-mitochondrial apoptosis pathway.