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RESEARCH ARTICLE
Year : 2015  |  Volume : 10  |  Issue : 3  |  Page : 481-489

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


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

Correspondence Address:
Jing Zhao
Institute of Neuroscience and Pathophysiology, Chongqing Medical University, Chongqing
China
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Source of Support: This study was supported by grants from the National Natural Science Foundation of China, No. 81171090; Natural Science Foundation of Chongqing Education Committee of China, No. KJ110313; Foundation of Key State Laboratory of Neurobiology of Fudan University in China, No. 10-08; and Foundation of Key Laboratory of Ministry of Education of the Third Medical Military University in China., Conflict of Interest: None


DOI: 10.4103/1673-5374.153700

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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.


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