Protective Effects of Gallic Acid Against NiSO(4)-Induced Toxicity Through Down-Regulation of the Ras/ERK Signaling Pathway in Beas-2B Cells

BACKGROUND: This study aimed to explore the preventive effects of gallic acid (GA) on the toxicity induced by NiSO(4) in Beas-2B cells. MATERIAL/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 NiSO(4) 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 NiSO(4). Western blot analysis demonstrated that NiSO(4) could up-regulate the related protein in the Ras/ERK signaling pathway. Furthermore, we observed that GA could alleviate the toxicity of NiSO(4) through regulating protein changes in the Ras/ERK signaling pathway. CONCLUSIONS: Preventive effects of GA on NiSO(4)-induced cytotoxicity in Beas-2B cells may be through the Ras/ERK signaling pathways.