Curcumin attenuates cerebral ischemia injury in Sprague-Dawley rats and PC12 cells by suppressing overactivated autophagy.

The present study assessed whether the protective effects of curcumin against cerebral ischemia injury were due to the suppression of overactivated autophagy. Curcumin is a well-known natural polyphenolic compound that effectively counteracts oxidation, inflammation, and various types of cancer. Several studies have demonstrated the protective effects of curcumin against ischemia-reperfusion injury in tissues from the lungs, cardiomyocytes, and liver. The present study employed brain injury models induced by middle cerebral artery occlusion (MCAO) in rats and PC12 oxygen-glucose-deprived (OGD) cells. Infarct area, neurological score, lactate dehydrogenase (LDH) activity, autophagy expression, cell apoptosis, and mRNA and protein expressions of caspase-3 were determined following curcumin supplementation. Compared to MCAO rats, curcumin-treated MCAO rats exhibited substantial reductions in neurological score, infarct area, and LDH activity. MCAO also increased LC3 II/I protein expression and decreased p62 protein expression, but curcumin supplementation significantly reversed these altered protein expressions. Caspase-3 protein expression increased by 46.2% in the MCAO group, but curcumin supplementation significantly reduced this expression. Similarly, apoptosis increased by 33.1% in OGD cells, but curcumin supplementation significantly reduced apoptosis to 21.6% and 9.3% at doses of 100 and 200 mg/kg, respectively. The mRNA and protein expressions of caspase-3 exhibited substantial increases in OGD cells but these expressions were significantly decreased following curcumin supplementation. Taken together, the present results indicate that curcumin represents a natural bioactive substance that can protect against cerebral ischemia via the suppression of overactivated autophagy.