Curcumin attenuates cerebral ischemia-reperfusion injury through regulating mitophagy and preserving mitochondrial function

Curcumin, the complex extracted from the traditional edible herb, has a wide range of pharmacological effects. A great deal of studies has demonstrated that curcumin could protect against cerebral ischemia-reperfusion (I/R) injury. In the present study, we aimed to test the hypothesis curcumin reduc...

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Bibliographic Details
Published inCurrent neurovascular research
Main Authors Wang, Weiwei, Xu, Jiaping
Format Journal Article
LanguageEnglish
Published United Arab Emirates 01.01.2020
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Summary:Curcumin, the complex extracted from the traditional edible herb, has a wide range of pharmacological effects. A great deal of studies has demonstrated that curcumin could protect against cerebral ischemia-reperfusion (I/R) injury. In the present study, we aimed to test the hypothesis curcumin reduces brain damage via regulating mitophagy and preserving mitochondrial function. To clarify the potential effect and mechanism of curcumin on cerebral I/R, we utilize MCAO followed by reperfusion rats and OGD/R neurons as cerebral I/R in vivo and in vitro, respectively. We determined the cellular ROS levels and mitochondrial function, including mitochondrial membrane potential (MMP), ATP levels, state 3 respiration and state 4 respiration. We also detected the levels of mitophagy by immunofluorescent staining and western blotting. Results found curcumin decreased neurological deficit scores, infarct volume and morphological changes of neurons in rats after brain I/R injury. Curcumin also reduced the levels of ROS while increased MMP, ATP levels and state 3 respiration to prevent the impairment of mitochondrial function from cerebral I/R. Furthermore, curcumin enhanced the co-localization of LC3B and mitochondrial marker VDAC1, the ratio of LC3-II to LC3-I, improving cerebral I/R-induced mitophagy. In conclusion, our results suggest that curcumin protects against cerebral I/R injury by improving mitophagy and preserving mitochondrial function.
ISSN:1875-5739
DOI:10.2174/1567202617666200225122620