ω-3不饱和脂肪酸通过影响自噬改善血管紧张素Ⅱ所致心肌细胞损伤

Omega-3 unsaturated fatty acids improve cardiomyocyte damage caused by angiotensin Ⅱby affecting autophagy

目的 心肌细胞的自噬受到非常精细地调节,本实验探讨ω-3不饱和脂肪酸是否能通过影响自噬改善心肌细胞损伤并深入研究其机制。方法 使用H9C2细胞系以及成年C57BL/6小鼠心肌细胞原代培养,将心肌细胞暴露于血管紧张素Ⅱ和ω-3不饱和脂肪酸环境中,检测心肌细胞结构稳定性和心肌细胞自噬状态,检测指标包括心肌细胞骨架蛋白α-Actinin变化情况变化、细胞自噬流水平变化及细胞自噬相关蛋白变化等。结果 血管紧张素Ⅱ诱导心肌细胞中α-Actinin纤维排列消失,变为散点状结构。ω-3多不饱和脂肪酸使心肌细胞α-Actinin纤维排列结构保持正常。血管紧张素Ⅱ可诱导心肌细胞自噬流明显上调(P<0.01),而ω-3多不饱和脂肪酸可抑制暴露于血管紧张素Ⅱ的H9c2细胞自噬水平(P<0.01)。血管紧张素Ⅱ提升细胞LC3Ⅱ/LC3Ⅰ表达,而ω-3多不饱和脂肪酸能够抑制LC3Ⅱ/LC3Ⅰ水平的升高。结论 ω-3多不饱和脂肪酸可通过调节自噬水平来减轻心肌细胞的结构损伤。

Objective Autophagy in cardiomyocytes is very finely regulated. The present study explored whether ω-3 unsaturated fatty acids could improve cardiomyocyte injury by affecting autophagy and its mechanism.Methods H9C2 cell line and primary culture of adult C57BL/6 mouse cardiomyocytes are used for experiments.Cardiac cells were exposed to angiotensin Ⅱ and Omega-3 unsaturated fatty acids. Autophagy and cell myofibril stabilization situation was detected. Detection indicators include changes in cardiac cytoskeletal protein α-Actinin,changes in autophagy flux levels, and changes in autophagy-related proteins. Results Angiotensin Ⅱinduction in cardiomyocytes α-The actinin fiber arrangement disappeared and became a scattered structure. ω-3 PUFAs prime cardiomyocytes α-Actinin fiber alignment structure remained normal. Autophagic flux in cardiomyocytes was significantly upregulated by angiotensin Ⅱ(P<0.01 ω-3 PUFA inhibited autophagy in H9c2 cells exposed to angiotensin Ⅱ(P<0.01). Angiotensin II elevated cellular lc3ii/lc3i expression, whereas ω-3 PUFAs can suppress the increase in lc3ii/lc3i levels. Conclusion Polyunsaturated fatty acids can reduce the structural damage of cardiomyocytes by regulating the level of autophagy.