牦牛血低聚肽对缺氧介导的H9c2心肌细胞损伤的保护及其作用机制

Effects of yak blood oligopeptides on hypoxia-induced injury of H9c2 cardiomyocytes protection and its mechanism

体外培养H9c2心肌细胞建立缺氧损伤模型,随机分为5组(n=6):正常对照组、缺氧组、牦牛血低聚肽低、中、高剂量组。结果表明,缺氧组的细胞存活率显著降低(P<0.01)、细胞凋亡率显著升高(P<0.01)、LDH释放水平显著升高(P<0.01),线粒体膜电位极显著降低(P<0.01),表明缺氧对H9c2心肌细胞产生了损伤。与缺氧组相比,牦牛血低聚肽干预组的细胞存活率增加,细胞凋亡减少以及细胞中LDH的释放水平下降,并呈良好的剂量依赖关系。同时,牦牛血低聚肽能够抑制线粒体膜电位下降,提高细胞T-AOC水平,降低TNF-α水平,抑制缺氧介导的细胞色素C的释放,上调抗凋亡蛋白(Survivin、p-Akt、Akt)的表达,降低促凋亡蛋白(Caspase-3/9)的活性,且牦牛血低聚肽也影响编码上述蛋白的m RNA水平。以上结果表明;牦牛血低聚肽对H9c2心肌细胞的保护与抑制PI3K-Akt信号转导通路、保护细胞线粒体结构功能完整性有密切关系。

To investigate the protective effect of yak blood oligopeptides on hypoxic injury of H9 c2 cardiomyocytes and its mechanism.The hypoxia injury model was established by culturing H9 c2 cardiomyocytes in vitro,randomly divided into 5 groups(n=6):normal control group,hypoxia group,low-dose yak blood oligopeptide group,middle-dose yak blood oligopeptide group and high-dose yak blood oligopeptide group.The results showed that:the cell survival rate of hypoxia group was significantly lower than that of control group(P<0.01),the rate of apoptosis was significantly increased(P<0.01),the release level of LDH was significantly increased(P<0.01),mitochondrial membrane potential decreased significantly(P<0.01),which showed that hypoxia could cause damage to H9 c2 cardiomyocytes.At the same time,compared with the anoxic group,yak blood oligopeptides could inhibit mitochondrial membrane potential decline,improved the T-AOC level of cells,reduced the level of TNF-α,inhibited the release of cytochrome C,upregulated the expression of anti-apoptotic proteins(Survivin,p-Akt,Akt),decreased the activity of apoptosis protein(Caspase-3/9),and affected the level of mRNA encoding of the above protein.The above results showed that the protective effect of yak blood oligopeptides on H9 c2 cardiomyocytes was closely related to the inhibition of PI3 K-Akt signal transduction pathway and the protection of mitochondrial structural and functional integrity.