Corilagin prevents tert-butyl hydroperoxide-induced oxidative stress injury in cultured N9 murine microglia cells |
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Authors: | Chen Yiyan Chen Chonghong |
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Affiliation: | a Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, Fujian, PR China b Department of Pharmacy, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, PR China |
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Abstract: | Oxidative stress plays an important role in neurodegenerative diseases. Reactive oxygen species (ROS)-mediated stress in microglia in vivo could result in cellular injuries and preferentially induces neuronal injury. Corilagin, a novel member of the phenolic tannin family, has been shown to possess antioxidant properties. In this study, we investigated the effects of corilagin on tert-butyl hydroperoxide (TBHP)-induced injury in cultured N9 murine microglial cells and the underlying mechanisms by a methyltetrazolium assay and oxidative damage assay. We found that exposure of N9 cells to TBHP induced cytotoxicity as demonstrated by cell shrinkage, loss of cell viability, increased lactate dehydrogenase (LDH) leakage, and increased intracellular levels of ROS. By contrast, TBHP reduced both superoxide dismutase activity and total cell anti-oxidation capacity, but glutathione was not reduced. Moreover, TBHP treatment was associated with the loss of mitochondrial membrane potential, and it induced cell apoptosis through the mitochondrial-mediated pathway involving the down-regulation of Bcl-2 expression and up-regulation of the Bax/Bcl-2 ratio. Interestingly, pre-treatment with corilagin reversed these reactions. These data collectively indicated that corilagin could attenuate TBHP-induced oxidative stress injury in microglial cells, and its protective effects may be ascribed to its antioxidant and antiapoptotic properties. Our findings suggest that corilagin should be a potential candidate for the treatment of oxidative stress-induced neurodegenerative diseases. |
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Keywords: | ROS, reactive oxygen species TBHP, tert-butyl hydroperoxide LDH, lactate dehydrogenase NAC, N-acetylcysteine MTT, methyltetrazolium DCFH-DA, 2&prime ,7&prime -dichlorodihydrofluorescein diacetate Rh 123, rhodamine 123 PI, propidium iodide DMEM, Dulbecco&rsquo s Modified Eagle&rsquo s medium SOD, superoxide dismutase T-AOC, total anti-oxidant capacity GSH, glutathione FBS, fetal bovine serum MMP, mitochondrial membrane potential DCF, 2&prime ,7&prime -dichlorofluorescein PVDF, polyvinylidene difluoride |
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