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首页> 外文期刊>Medical science monitor : >Protective Effects of Gallic Acid Against NiSO4-Induced Toxicity Through Down-Regulation of the Ras/ERK Signaling Pathway in Beas-2B Cells
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Protective Effects of Gallic Acid Against NiSO4-Induced Toxicity Through Down-Regulation of the Ras/ERK Signaling Pathway in Beas-2B Cells

机译：没食子酸通过下调Beas-2B细胞Ras / ERK信号通路对NiSO4诱导的毒性的保护作用。

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BACKGROUND This study aimed to explore the preventive effects of gallic acid (GA) on the toxicity induced by NiSO4 in Beas-2B cells. MATERIAL AND METHODS Beas-2B cell viability was measured by MTT assay. The degree of oxidative stress was detected by measuring the levels of reactive oxygen species (ROS) and lipid peroxide (LPO). The rate of apoptosis was measured by flow cytometry. Ras/ERK-related protein levels were analyzed by Western blot analysis, which including Ras, ERK, c-Myc, PARP, and PARP cleavage. RESULTS MTT assay showed that NiSO4 induced cytotoxicity, while GA had a protective role against toxicity. Additionally, GA could reduce the apoptotic cell number and the level of ROS in Beas-2B cells induced by NiSO4. Western blot analysis demonstrated that NiSO4 could up-regulate the related protein in the Ras/ERK signaling pathway. Furthermore, we observed that GA could alleviate the toxicity of NiSO4 through regulating protein changes in the Ras/ERK signaling pathway. CONCLUSIONS Preventive effects of GA on NiSO4-induced cytotoxicity in Beas-2B cells may be through the Ras/ERK signaling pathways.
机译：背景技术本研究旨在探讨没食子酸（GA）对NiSO4诱导的Beas-2B细胞毒性的预防作用。材料与方法用MTT法测定Beas-2B细胞的活力。通过测量活性氧（ROS）和脂质过氧化物（LPO）的水平来检测氧化应激的程度。通过流式细胞术测量细胞凋亡率。 Ras / ERK相关蛋白水平通过蛋白质印迹分析进行了分析，包括Ras，ERK，c-Myc，PARP和PARP裂解。结果MTT分析表明NiSO4诱导了细胞毒性，而GA具有抗毒性作用。此外，GA可以减少NiSO4诱导的Beas-2B细胞的凋亡细胞数量和ROS水平。 Western blot分析表明，NiSO4可以上调Ras / ERK信号通路中的相关蛋白。此外，我们观察到GA可以通过调节Ras / ERK信号通路中的蛋白质变化来减轻NiSO4的毒性。结论GA对Beas-2B细胞NiSO4诱导的细胞毒性的预防作用可能是通过Ras / ERK信号通路。

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