黑青稞籽皮提取物对心肌细胞缺氧/复氧损伤的保护作用

目的研究黑青稞籽皮提取物对心肌细胞缺氧／复氧（H／R）损伤的保护作用及其机制。方法取大鼠胚胎心肌细胞（H9c2），随机分为5组：正常对照组（C组）、缺氧／复氧组（H／R组）、缺氧／复氧＋低、中、高剂量药物组（H／R＋L、M、H组）。流式细胞术检测细胞凋亡、细胞线粒体跨膜电位（Aaltm）和细胞内活性氧（ROS）产生情况；Westernblot方法检测B细胞淋巴瘤／白血病-2基因（Bcl-2），Bcl-2相关X蛋白（Bax），总丝氨酸苏氨酸蛋白激酶（tAkt）和磷酸化丝氨酸／苏氨酸蛋白激酶（pAkt）蛋白表达变化。结果药物组[H／R＋L）组至（H／R＋H组）】细胞凋亡比例为（26．7±2．9）％至（6．1±1．1）％，较H／R组[（57．3-＋10．4）％1明显降低，差异有统计学意义（P〈0．05）；与H／R组比较，药物组△ψm升高，差异有高度统计学意义（P〈0．01），ROS水平下降，差异有高度统计学意义（P〈0．01），Bcl-2及pAkt表达升高，Bax及tAkt表达无明显变化。结论黑青稞籽皮提取物对心肌细胞缺氧／复氧损伤具有保护作用，可抑制心肌细胞凋亡．其可能与Bcl一2／13ax调控和激活磷脂酰肌醇一3激酶／丝氨酸苏氨酸蛋白激酶（P13K-Akt）信号通路有关。

Protective effect of black barley pericarp extract on cardiomyocytes a- gainst hypoxia/reoxygenation injury

Objective To investigate the protective effect of black barley pericarp extract on cardiomyocytes against hy- poxia/reoxygenation injury and to elucidate its underlying mechanism. Methods Cultured rat cardiac myoblast cells H9c2 were randomly divided into 5 groups： normal control group （C group）, hypoxia/reoxygenation injury group （H/R group）, and H/R followed by drug treatment with low/median/high dose group （HR＋L, ＋M, ＋H group）. Cell apoptosis, mitoehondrial transmembrane potential （Aψm） and the generation of intracellular ROS were monitored by flow cytome- ter. The protein levels of Bel-2, Bax, tAkt and pAkt in H9e2 cells were observed by Western blot assay. Results It was shown that black barley pericarp extract could reduce the apoptosis rate compared with H/R group cells [H/R group： （57.3＋10.4）%, drug treat group （H/R＋L） group--＊（H/R＋H） group： （26.7＋2.9）% to （6.1＋1.1）%, P 〈 0.05], rescue the loss of mitochondrial transmembrane potential （P 〈 0.01）, and inhibit the production of ROS （P 〈 0.01）. Drug treatments in- creased the expression levels of Bcl-2 and pAkt rather than H/R group cells, accompanied with no changes in the ex- pression levels of Bax and tAkt. Conclusion Black barley periearp extract can protect eardiomyocytes against hypoxia/ reoxygenation injury and suppress the apoptosis of cardiomyoeytes, which may relate to Bcl-2/Bax regulation and PI3K-Akt activation pathway.