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Qishen Yiqi Drop Pill, a novel compound Chinese traditional medicine protects against high glucose‐induced injury in cardiomyocytes

机译:七神益气滴丸,一种新型的中药复方,可预防高糖诱导的心肌细胞损伤

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Objective Qishen Yiqi Drop Pill (QSYQ) has been recognized as a potential protective agent for various cardiovascular diseases. However, the effect of QSYQ in cardiac complications associated with diabetes is not clear currently. In this study, we investigate whether QSYQ could exert cardiac protective effects against high glucose‐induced injuries in cardiac H9c2 cells. Methods H9c2 cells were exposed to 24?hours of high glucose in presence or absence of QSYQ and LY294002. Cell cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were determined. Levels of bax, bcl‐2, p53, cleaved caspase‐3, PI3K and Akt were evaluated by Western blot. Results Our data indicated that QSYQ significantly increased the cell viability and decreased cytotoxicity. By analysing the apoptotic rate as well as the expression levels of cytoapoptosis‐related factors including cleaved caspase‐3, bax, bcl‐2, and p53, we found that QSYQ could remarkably suppress apoptosis of cardiomyoblasts caused by high glucose. In addition, it also showed that QSYQ reduced the generation of ROS. We further found that QSYQ treatment could inhibit the loss of mitochondrial membrane potential and mPTP opening. Moreover, Western blot analysis showed enhanced phosphorylation of PI3K/Akt. The specific inhibitor of PI3K, LY294002 not only inhibited QSYQ induced PI3K/Akt signalling pathway activation, but alleviated its protective effects. Conclusions In summary, these findings demonstrated that QSYQ effectively protected H9c2 cells against the series injuries due to high glucose at least partially by activating the PI3K/Akt signalling pathway.
机译:目的芪参益气滴丸(QSYQ)被公认为是多种心血管疾病的潜在保护剂。但是,目前尚不清楚QSYQ在与糖尿病有关的心脏并发症中的作用。在这项研究中,我们调查QSYQ是否可以对心脏H9c2细胞中高糖诱导的损伤发挥心脏保护作用。方法在存在或不存在QSYQ和LY294002的情况下,将H9c2细胞暴露于24小时高血糖。测定细胞的细胞毒性,细胞凋亡,活性氧(ROS)生成,线粒体膜电位和线粒体通透性转换孔(mPTP)开口。通过蛋白质印迹评估bax,bcl-2,p53,裂解的caspase-3,PI3K和Akt的水平。结果我们的数据表明,QSYQ显着增加了细胞活力并降低了细胞毒性。通过分析细胞凋亡率以及细胞凋亡相关因子(包括裂解的caspase-3,bax,bcl-2和p53)的表达水平,我们发现QSYQ可以显着抑制高葡萄糖引起的成肌细胞凋亡。此外,这也表明QSYQ减少了ROS的生成。我们进一步发现QSYQ处理可以抑制线粒体膜电位的丧失和mPTP的开放。而且,蛋白质印迹分析显示PI3K / Akt的磷酸化增强。 PI3K的特异性抑制剂LY294002不仅抑制QSYQ诱导的PI3K / Akt信号通路活化,而且减轻了其保护作用。结论总之,这些发现证明QSYQ至少部分地通过激活PI3K / Akt信号通路有效地保护了H9c2细胞免受高糖引起的系列损伤。

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