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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(ΔΨm)和细胞内活性氧(ROS)产生情况;Western blot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)%]明显降低,差异有统计学意义(P<0.05);与H/R组比较,药物组ΔΨm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-2/Bax调控和激活磷脂酰肌醇-3激酶/丝氨酸苏氨酸蛋白激酶(PI3K-Akt)信号通路有关。
Objective To study the protective effect and its mechanism of extract of black sesame seed on cardiac myocyte hypoxia / reoxygenation (H / R) injury. Methods Rat embryonic cardiomyocytes (H9c2) were randomly divided into 5 groups: normal control group (C group), hypoxia / reoxygenation group (H / R group), hypoxia / reoxygenation + low, middle and high dose Drug group (H / R + L, M, H group). Flow cytometry was used to detect cell apoptosis, mitochondrial transmembrane potential (ΔΨm) and intracellular reactive oxygen species (ROS) production; Western blot was used to detect Bcl-2, Bcl-2 Related X protein (Bax), total serine threonine protein kinase (tAkt) and phosphorylated serine / threonine protein kinase (pAkt) protein expression changes. Results The percentage of apoptotic cells in the H / R + H group was (26.7 ± 2.9)% vs (6.1 ± 1.1)% in the H / R group compared with that in the H / R group [(57.3 ± (P <0.05). Compared with the H / R group, the ΔΨm in the drug group was significantly increased (P <0.01), and the ROS level was decreased with a significant difference Statistical significance (P <0.01), Bcl-2 and pAkt expression increased, Bax and tAkt expression did not change significantly. Conclusion The extract of black sesame seed extract can protect cardiomyocytes against hypoxia / reoxygenation injury and inhibit cardiomyocyte apoptosis. It may be related to the regulation and activation of phosphatidylinositol 3-kinase / serine threonine by Bcl-2 / Bax Protein kinase (PI3K-Akt) signaling pathway.