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作 者:关婉辰 戴璐彬 张栋[1] 周凯旋 刘佳[1] 鲍慧玮 李丽静[1] GUAN Wan-Chen;DAI Lu-Bin;ZHANG Dong(Changchun University of Chinese Medicine,Changchun 130117,Jilin,China)
出 处:《中国老年学杂志》2022年第9期2211-2215,共5页Chinese Journal of Gerontology
基 金:国家自然科学基金(81274036);国家级大学生创新创业训练计划项目(202110199005);吉林省中医药管理局课题(2019047);长春中医药大学校内基金(2019012)。
摘 要:目的探究参麦方对大鼠心肌细胞糖脂毒性损伤的影响。方法建立体外糖脂毒性对心肌细胞损伤模型,CCK8法检测细胞存活率;Western印迹检测心肌细胞的磷脂酰肌醇-3激酶(PI3K)、磷酸化(p)-蛋白激酶B(AKT)/AKT、p-雷帕霉素靶蛋白(mTOR)/mTOR蛋白表达;Hoechst33258观察凋亡染色;Western印迹检测凋亡相关蛋白B细胞淋巴瘤(Bcl)-2、Bcl-2相关X蛋白(Bax)、活性半胱天冬酶(Cleaved-Caspase)3表达。结果0.40 mmol/L棕榈酸和30 mmol/L葡萄糖条件下损伤程度可缓解,实验重复性稳定,证明心肌细胞糖脂毒性模型造模成功;与模型组比较,各给药组PI3K、p-AKT/AKT蛋白显著上调,p-mTOR/mTOR蛋白显著下调;模型组玻珠样病变增多,核质发生皱缩,给药后与模型组比较,玻珠样病变减少。与模型组比较,各给药组促凋亡蛋白Bax、Cleaved-Caspase3显著下调,抗凋亡蛋白Bcl-2显著上调(P<0.05,P<0.01)。结论初步验证参麦方对糖脂毒性损伤的心肌细胞具有保护作用,参麦方可能激活了PI3K/AKT/mTOR通路,调控相关凋亡蛋白,减少心肌细胞凋亡从而改善心肌细胞损伤。Objective To explore the effect of shenmai recipe on the glycolipid toxicity injury of cultured rat myocardial cells.Methods A glycolipid toxic injury model of myocardial cells was established in vitro.CCK8 method was used to detect cell viability;the protein expression of PI3K,p-AKT/AKT and p-mTOR/mTOR in cardiomyocytes were detected by Western blot;Hoechst33258 staining was used to observe cell apoptosis;the expression of apoptosis-related proteins Bax,Bcl-2 and Cleaved-Caspase3 were detected by Western blot.Results The degree of damage was alleviated under 0.40 mmol/L palmitate and 30 mmol/L glucose,the reproducibility of the experiment was stable,the model of glycolipid toxicity of cardiomyocytes was successfully established;compared with model group,PI3K and p-AKT/AKT protein were up-regulated and p-mTOR/mTOR protein was down-regulated in all drug administration groups;in the model group,there were more glass-like lesions and nuclear shrinkage,compared with model group,hyaline lesions were reduced in each administration group.Compared with model group,pro-apoptotic proteins Bax and Cleaved-Caspase3 were significantly down-regulated,and anti-apoptotic protein Bcl-2 was significantly up-regulated in each administration group(P<0.05,P<0.01).Conclusions It is preliminarily verified that shenmai recipe has a protective effect on cardiomyocytes injured by glycolipid toxicity,which may be related to activating the PI3K/AKT/mTOR pathway,regulating apoptosis-related proteins,reducing cell apoptosis,and improving myocardial function.
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