Abstract

Tetrahydroxystilbene Glucoside Exerts Cytoprotective Effect against Hydrogen Peroxide-induced Cell Death Involving ROS Production and Antioxidant Enzyme Activation

Author(s): S. S. Tian, P. Song1, L. Y. Liu, R. Zhu and H. J. Zhao*
Institute of Pharmacology, College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310053, 1The Second Affiliated hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310001, China

Correspondence Address:
Institute of Pharmacology, College of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310053, China. [email protected]


Epithelial injury caused by reactive oxygen species including hydrogen peroxide plays a critical role in the pathogenesis of gastric disorders. Tetrahydroxystilbene glucoside is an active component extracted from Polygonum multiflorum, a famous traditional Chinese herb. This study aimed to evaluate the protective effect of tetrahydroxystilbene glucoside on hydrogen peroxide-induced oxidative stress on non-malignant gastric epithelial cells and to see if these protective actions can be extended to gastric cancer cells. The results from MTT assay showed that incubating gastric epithelial cells and gastric cancer cells with 200 μΜ hydrogen peroxide for 24 h significantly decreased cell viability, whereas pre-incubating cells with 10 μΜ tetrahydroxystilbene glucoside for 24 h protected the cells against hydrogen peroxide cell damage, and more significantly in gastric epithelial cells. Using 2′,7′-dichlorofluorescin diacetate, we found that tetrahydroxystilbene glucoside inhibited the production of intracellular reactive oxygen species in gastric epithelial cells and gastric cancer cells. In addition, it induced the expression of antioxidant enzymes hemeoxygenase-1 and NADPH quinone oxidoreductase-1. These results demonstrated that tetrahydroxystilbene glucoside exerted stronger cytoprotective effect against peroxide-induced cell death in gastric epithelial cells than gastric cancer cells and the cytoprotective mechanisms might be through decreasing oxidative stress and activating the expression of hemeoxygenase-1 and NADPH quinone oxidoreductase-1.



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