羟基红花黄色素调节Sirt 3改善心脏缺血再灌注损伤中线粒体功能障碍  

Hydroxy-safflower yellow A improves mitochondrial dysfunction in myocardial ischemia reperfusion injury by regulating SIRT3

作　　者：王永贤 刘军利 高景峰[2] 霍涛[3] 许立刚[3] WANG Yongxian;LIU Junli;GAO Jingfeng(Catheterization Department,Shijiazhuang People’s Hospital,Hebei,Shijiazhuang 050000,China;不详)

机构地区：[1]河北省石家庄市人民医院导管室,050000 [2]河北省唐山市丰润区人民医院CT室 [3]河北省保定市第三中心医院

出　　处：《河北医药》2024年第18期2737-2741,共5页Hebei Medical Journal

摘　　要：目的探讨羟基红花黄色素对脂多糖诱导的H9c2心肌细胞损伤线粒体功能保护作用及其对Sirt3的调节作用。方法H9c2心肌细胞株培养24 h后随机分为对照组、脂多糖造模组、脂多糖造模+Sirt3抑制剂组,羟基红花黄色素给药+模型组,羟基红花黄色素给药+Sirt 3抑制剂+模型组,给予脂多糖建立氧化应激损伤心肌细胞模型。采用乳酸脱氢酶检测试剂盒测定细胞培养液中乳酸脱氢酶含量;测定细胞中ATP含量,测定细胞中细胞色素C含量及线粒体呼吸链复合物含量;Western blot法检测Sirt 3及Bax表达量。结果与对照组比较,脂多糖模型组细胞色素C含量升高,细胞中谷氨酸脱氢酶,ATP及呼吸链复合物含量降低,Sirt3表达量略升高,Bax表达上升(P<0.05)与模型组比较,脂多糖造模+Sirt3抑制组线粒体各项损失指标明显加剧,而羟基红花黄色素给药+模型组中线粒体损伤指标明显恢复(P<0.05),而羟基红花黄色素+Sirt 3抑制剂组中线粒体损伤程度低于脂多糖造模+Sirt3抑制剂组(P<0.05),Sirt3蛋白表达较抑制组明显上升(P<0.05)。结论羟基红花黄色素降低脂多糖诱导的H9c2心肌细胞线粒体氧化损伤,该作用可能与羟基红花黄色素提高受损心肌细胞内Sirt3的表达量有关。Objective To investigate the protective effect of hydroxy-safflower yellow A(HSYA)on the mitochondrial function in the myocardial cell line H9c2 induced by lipopolysaccharide(LPS)and its regulation on SIRT3.Methods H9c2 cells were cultured for 24 h,and treated with control,LPS induction,LPS induction+SIRT3 inhibitor,HSYA+LPS induction,and HSYA+LPS induction+SIRT3 inhibitor.LPS induction was performed in H9c2 cells to create the in vitro oxidative stress model in cardiomyocytes.Lactate dehydrogenase detection kit was used to determine the content of lactate dehydrogenase in the culture medium.The contents of adenosine triphosphate(ATP),cytochrome C and mitochondrial respiratory chain complex in cells were measured.The protein expressions of SIRT3 and Bax were detected by Western blot.Results Compared with those treated with control,LPS induction significantly increased the contents of cytochrome C and glutamate dehydrogenase in cells,and significantly decreased ATP and respiratory chain complex.Meanwhile,LPS induction slightly upregulated SIRT3 and significantly upregulated Bax.Compared with those induced with LPS,mitochondrial dysfunction indicators were significantly pronounced in LPS-induced H9c2 cells treated with SIRT3 inhibitor,which were significantly reversed by the treatment of HSYA.The degree of mitochondrial dysfunction was lower in H9c2 cells treated with LPS+HSYA+SIRT3 inhibitor than those treated with LPS+SIRT3 inhibitor,and SIRT3 was upregulated in the former group.Conclusion HSYA can reduce mitochondrial oxidative damage in LPS-induced H9c2 cells by upregulating SIRT3 in injured cardiomyocytes.

关 键 词：羟基红花黄色素 Sirt 3 线粒体呼吸链复合物 线粒体功能障碍 

分 类 号：R54[医药卫生—心血管疾病]