红花黄素A调控核受体TR3胞内移位抑制氧化应激对心肌细胞的损伤  

Safflor yellow A inhibits oxidative stress on cardiomyocyte via regulation of nuclear receptor TR3 localization

作　　者：骆杰炉[1] 梁俭[1] 梁文能[1] LUO Jie-lu;LIANG Jian;LIANG Wen-neng(Department of Pharmacy,The First Hospital Affiliated to Guangzhou University of TCM,Guangzhou 510405,China)

机构地区：[1]广州中医药大学第一附属医院药学部,广东广州510405

出　　处：《中成药》2020年第6期1462-1467,共6页Chinese Traditional Patent Medicine

摘　　要：目的探究红花黄素A调控核受体TR3胞内移位抑制氧化应激对心肌细胞的损伤。方法利用H2O2诱导H9c2心肌细胞建立心肌氧化应激模型,不同浓度红花黄素A处理H2O2诱导H9c2心肌细胞24 h,CCK-8法检测心肌细胞存活率,流式细胞法检测心肌细胞凋亡率,比色法检测SOD、MDA水平,免疫荧光法观察TR3在细胞内的定位,Western blot法检测TR3在细胞核和线粒体表达以及凋亡通路蛋白Bcl-2、Bax、cl caspase-9表达。结果与模型组相比,红花黄素A增加H9c2心肌细胞存活率,降低细胞凋亡率,升高SOD水平,降低MDA水平,促进Bcl-2蛋白表达,抑制Bax、cl caspase-9蛋白表达(P<0.05,P<0.01),呈浓度依赖性。随着红花黄色素A的浓度增加,TR3核受体的移位逐渐减小并聚集在细胞核附近。结论红花黄素A能够调控核受体TR3从细胞核向线粒体的转移,并通过抑制线粒体凋亡通路,从而减轻氧化应激对心肌细胞的损伤。AIM To study safflor yellow A’s inhibition on oxidative stress of cardiomyocyte via regulation of nuclear receptor TR3 localization.METHODS H2O2-injured H9 c2 myocardial cells were established as myocardial oxidative stress models for 24 h treatment of different concentrations of safflor yellow A. The cells were subjected to tests of the rate of myocardial cell viability by CCK-8 kit, the rate of myocardial cell apoptosis by flow cytometry, the levels of SOD and MDA by colorimetry, TR3 localization in cells by immunofluorescence, TR3 expression in the nucleus and mitochondria and the expression of apoptosis pathway proteins Bcl-2, Bax and cl caspase-9 by Western blot.RESULTS Compared with the model group, the goups treated with safflor yellow A shared concentration-dependently increase in the survival rate of H9 c2 cardiomyocytes, decrease in the apoptosis rate, reduction in the level of MDA, increase the level of SOD, promotion of the expression of Bcl-2 protein, and inhibition in the expression of Bax and cl caspase-9 protein(P<0.05, P<0.01). The increase of safflor yellow A concentration brought forth TR3 nuclear receptors’ gradual translocation decrease, and their accumulation near the nucleus.CONCLUSION Inhibiting the nuclear receptor TR3 transfering from nucleus to mitochondria and affecting the mitochondrial apoptotic pathway via oxidative stress response reduction, safflor yellow A can thus alleviate oxidative stress-induced damage of myocardial cells.

关 键 词：红花黄素A TR3核受体 氧化应激 心肌损伤 线粒体凋亡 

分 类 号：R285􀆰[医药卫生—中药学]