Curcumin Attenuates Cerebral Ischemia-reperfusion Injury Through Regulating Mitophagy and Preserving Mitochondrial Function

Background: 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 (UR) injury. In the present study, we aimed to test the hypothesis that curcumin reduces brain damage via regulating mitophagy and preserving mitochondrial function. To clarify the potential effect and mechanism of curcumin on cerebral UR, we utilize MCAO followed by reperfusion rats and OGD/R neurons as cerebral UR in vivo and in vitro, respectively. Methods: 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: Results found that curcumin decreased neurological deficit scores, infarct volume and morphological changes of neurons in rats after brain UR 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 UR. Furthermore, curcumin enhanced the co-localization of LC3B and mitochondria' marker VDAC1, the ratio of LC3-II to LC3-I, improving cerebral I/R-induced mitophagy. Conclusion: In conclusion, our results suggest that curcumin protects against cerebral UR injury by improving mitophagy and preserving mitochondrial function.