Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF‑κB, ICAM-1, MMP-9 and caspase-3 expression.

Abstract

Reperfusion is the only approved therapy for acute ischemic stroke; however, it can cause excessive inflammation responses and aggravate brain damage. Therefore, supplementary treatment against inflammation caused by reperfusion is required. In a previous study from our group, curcumin was demonstrated to decrease infarction volume, brain edema and blood-brain barrier (BBB) disruption against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanisms remain unclear. The present study was conducted to understand whether curcumin protects against cerebral I/R injury through anti-inflammatory and antiapoptotic properties. Ischemia for 1 h was induced in vivo in Wistar rats by middle cerebral artery occlusion (MCAO), followed by reperfusion for 24 h, and curcumin was injected intraperitoneally at 30 min prior to reperfusion. Immunohistochemistry was performed to analyze the expression levels of nuclear factor (NF)-κB, intercellular adhesion molecule (ICAM)-1, matrix metalloproteinase (MMP)-9 and caspase-3. The findings revealed that inflammation (NF-κB, ICAM-1 and MMP-9) and apoptosis (caspase-3)-related markers were significantly downregulated in the curcumin-treated MCAO group compared with the vehicle-treated MCAO group. Furthermore, brain infarction size, brain edema and neurological dysfunction were attenuated in the curcumin-treated MCAO group compared with the vehicle-treated MCAO group. Taken together, the present results provided evidence that the protective effect of curcumin against cerebral I/R injury might be mediated by anti-inflammatory and anti-apoptotic properties. Therefore, curcumin may be a promising supplementary agent against cerebral I/R injury in the future.