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Protective effect and its mechanism of curcumin on ischemia-reperfusion injury of cerebral cortex in rats

Medical Journal of Chinese People's Liberation Army. 2013;38(3):190-194


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Journal Title: Medical Journal of Chinese People's Liberation Army

ISSN: 0577-7402 (Print)

Publisher: Editorial Board of Medical Journal of Chinese People's Liberation Army

Society/Institution: Department of Health, Chinese People's Liberation Army

LCC Subject Category: Medicine: Medicine (General)

Country of publisher: China

Language of fulltext: Chinese

Full-text formats available: PDF




Bo-tao TAN


Gang YU


Peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 18 weeks


Abstract | Full Text

Objective  To investigate the effect of curcumin pretreatment on the expression of uncoupling protein 2 (UCP2) and mitochondrial transcription factor A (MTFA) in rats' cerebral cortex against focal ischemia reperfusion injury. Methods  Eighty male SD rats weighed 220g–300g were randomly divided into 4 groups: sham-operated group, ischemia/reperfusion (I/R) group, curcumine 50mg/kg+I/R (low dose) group, and curcumine 100mg/kg+I/R (high dose) group. The common carotid artery, external carotid artery and internal carotid artery on the right side were exposed in the sham-operated group. Animals of the other groups were subjected to a 2-hour period of right middle cerebral artery occlusion, followed by 24 hours of reperfusion, and then they were sacrificed. Curcumin was administered (ip) in a dose of 50mg/kg (low dose group) or 100mg/kg (high dose group) for 5 days, respectively, prior to arterial occlusion. The pathological changes in neurons and their mitochondria in the cerebral cortex supplied by middle cerebral artery were observed with Nissl staining and electron microscope, respectively. The expressions of UCP2 and MTFA in corresponding cotex were assessed by immunohistochemistry and RT-PCR. Results  Compared with sham-operated group, animals in I/R group presented edema of neurons in the corresponding cortex, reduction in the number of Nissl bodies, and swelling of mitochondria with broken, even lysis of cristae. Low dose and high dose of curcumin pretreatment before brain ischemia significantly alleviated the loss of neurons and the damage of mitochondria, accompanied with an increase in the expression of UCP2 and TFAM (P<0.05), and the changes appeared a dose-dependent manner (P<0.05). Conclusions  Curcumin may prevent neurons from focal cerebral ischemia reperfusion injury by up-regulating UCP2 and MTFA. Regulation of mitochondrial biogenesis may probably be a potential target of curcumin as a neuroprotective drug.