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首页> 外文期刊>Revista Brasileira de Farmacognosia >Protective effect of Rheum turkestanikum root against doxorubicin-induced toxicity in H9c2 cells
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Protective effect of Rheum turkestanikum root against doxorubicin-induced toxicity in H9c2 cells

机译:大黄大黄根对阿霉素诱导的H9c2细胞毒性的保护作用

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摘要

Doxorubicin is a chemotherapy drug but its clinical using is limited because of its cardiotoxicity. Reactive oxygen species play an important role in the pathological process. The aim of this study is to evaluate the protective effect of Rheum turkestanicum Janisch., Polygonaceae, against doxorubicin-induced apoptosis and death in H9c2 cells. The cells were incubated with different concentrations of R. turkestanicum extract and N -acetylcysteine as positive control for 2 h, followed by incubation with 5 ?μM doxorubicin for 24 h. Cell viability and apoptotic induction were determined by using MTT and PI assays, respectively. The level of reactive oxygen species and lipid peroxidation was measured by fluorimetric methods. Doxorubicin significantly decreased cell viability which was accompanied by an increase in ROS production and lipid peroxidation. Pretreatment with R. turkestanicum increased the viability of cardiomyocytes and could decrease lipid peroxidation and reactive oxygen species generation. Also, R. turkestanicum attenuated apoptotic induction. N -acetylcysteine at 100 ?μM reduced the levels of reactive oxygen species and lipid peroxidation. But, treating H9c2 cells with N -acetylcysteine did little to protect H9c2 cells from doxorubicin-induced cell death. R. turkestanicum exerts protective effect against oxidative stress-induced cardiomyocytes damage. Our findings showed that R. turkestanicum could exert the cardioprotective effects against doxorubicin-induced toxicity partly by anti-apoptotic activity. Also, N -acetylcysteine prevented oxidative stress via reduction of reactive oxygen species and lipid peroxidation. N -acetylcysteine induced less protective effects than R. turkestanicum extract against doxorubicin-induced cytotoxicity.
机译:阿霉素是一种化学治疗药物,但由于其心脏毒性,其临床应用受到限制。活性氧在病理过程中起重要作用。这项研究的目的是评估杜鹃花大黄大黄对阿霉素诱导的H9c2细胞凋亡和死亡的保护作用。将细胞与不同浓度的土耳其草提取物和N-乙酰半胱氨酸作为阳性对照孵育2小时,然后与5μM阿霉素孵育24小时。细胞活力和凋亡诱导分别通过使用MTT和PI测定来确定。通过荧光法测量活性氧和脂质过氧化的水平。阿霉素显着降低了细胞活力,并伴随着ROS产生和脂质过氧化的增加。土库曼斯坦罗克斯坦预处理可以增加心肌细胞的活力,并可以减少脂质过氧化作用和活性氧的产生。此外,土库曼斯坦R.减弱凋亡诱导作用。 100 µM的N-乙酰半胱氨酸降低了活性氧和脂质过氧化的水平。但是,用N-乙酰半胱氨酸处理H9c2细胞几乎没有保护H9c2细胞免受阿霉素诱导的细胞死亡。土库曼斯坦R. turkestanicum对氧化应激诱导的心肌细胞损害具有保护作用。我们的研究结果表明,土库曼斯坦R. turkstanicum可以通过抗凋亡活性部分发挥对阿霉素诱导的毒性的心脏保护作用。另外,N-乙酰半胱氨酸通过减少活性氧和脂质过氧化作用来防止氧化应激。 N-乙酰半胱氨酸对阿霉素诱导的细胞毒性的保护作用低于土耳其草提取物。

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