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.