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Mol Vis. 2010 Aug 4;16:1467-74.

Resveratrol protects human lens epithelial cells against H2O2-induced oxidative stress by increasing catalase, SOD-1, and HO-1 expression.

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Department of Ophthalmology, The First Affiliated Hospital of Harbin Medical University, Harbin, PR China.



Oxidative damage induced by H(2)O(2) treatment can irreversibly damage the lens epithelium, resulting in cell death and cataract. Whether the effects of oxidative stress could be attenuated in cultured human lens epithelial cells by incubation with resveratrol (RES) is still unknown. In the present study, we examined the function of resveratrol in protecting human lens epithelial B-3 (HLEB-3) cells against H(2)O(2) induced cell death and cell apoptosis, its role in reducing H(2)O(2) induced intracellular reactive oxygen species (ROS) accumulation, and investigated the mechanism by which resveratrol underlies the effect.


HLEB-3 cells, a human lens epithelial cell line, were exposed to 100 muM H(2)O(2) with or without RES pre-treatment at different concentrations for different time duration. Cell viabilities were monitored by 4-[3-[4-iodophenyl]-2-4(4-nitrophenyl)-2H-5-tetrazolio-1,3-benzene disulfonate] (WST-1) assay. The apoptosis rate and ROS generation were detected by flow cytometric analysis. Expression levels of superoxide dismutases-1 (SOD-1), catalase, and heme oxygenase-1 (HO-1) proteins were measured by western-blotting analysis. p38 and c-jun N terminal kinase (JNK) activation was also evaluated by western-blotting analysis.


Resveratrol clearly reduced H(2)O(2) induced cell apoptosis and ROS accumulation; protected HLEB-3 cells from H(2)O(2) induced oxidative damage, and increased the expression levels of SOD-1, catalase, and HO-1. Further studies showed that RES also inhibited H(2)O(2) induced p38 and JNK phosphorylation.


These findings suggested that RES protected HLEB-3 cells from H(2)O(2) induced oxidative damage, presumably by inducing three antioxidative enzymes including catalase, SOD-1, and HO-1.

[Indexed for MEDLINE]
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