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Neural Regen Res. 2015 Mar;10(3):481-9. doi: 10.4103/1673-5374.153700.

Curcumin pretreatment and post-treatment both improve the antioxidative ability of neurons with oxygen-glucose deprivation.

Author information

1
Department of Pathology, Chongqing Medical University, Chongqing, China ; Institute of Neuroscience, Chongqing Medical University, Chongqing, China.
2
Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China.
3
Institute of Neuroscience, Chongqing Medical University, Chongqing, China ; Department of Pathophysiology, Chongqing Medical University, Chongqing, China.

Abstract

Recent studies have shown that induced expression of endogenous antioxidative enzymes thr-ough activation of the antioxidant response element/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway may be a neuroprotective strategy. In this study, rat cerebral cortical neurons cultured in vitro were pretreated with 10 μM curcumin or post-treated with 5 μM curcumin, respectively before or after being subjected to oxygen-glucose deprivation and reoxygenation for 24 hours. Both pretreatment and post-treatment resulted in a significant decrease of cell injury as indicated by propidium iodide/Hoechst 33258 staining, a prominent increase of Nrf2 protein expression as indicated by western blot analysis, and a remarkable increase of protein expression and enzyme activity in whole cell lysates of thioredoxin before ischemia, after ischemia, and after reoxygenation. In addition, post-treatment with curcumin inhibited early DNA/RNA oxidation as indicated by immunocytochemistry and increased nuclear Nrf2 protein by inducing nuclear accumulation of Nrf2. These findings suggest that curcumin activates the expression of thioredoxin, an antioxidant protein in the Nrf2 pathway, and protects neurons from death caused by oxygen-glucose deprivation in an in vitro model of ischemia/reperfusion. We speculate that pharmacologic stimulation of antioxidant gene expression may be a promising approach to neuroprotection after cerebral ischemia.

KEYWORDS:

NSFC grant; brain injury; cortical neurons; curcumin; ischemia/reperfusion injury; nerve regeneration; neural regeneration; oxidative stress; oxygen-glucose deprivation; post-treatment; pretreatment; primary cell culture

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