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 (I/R) 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 I/R,
we utilize MCAO followed by reperfusion rats and OGD/R neurons as cerebral I/R in vivo and in
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 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/Rinduced
Conclusion: In conclusion, our results suggest that curcumin protects against cerebral I/R injury
by improving mitophagy and preserving mitochondrial function.