Cerebral ischemia and reperfusion was established through the classic middle cerebral artery occlusion (MCAO) for 2 h, followed by 24 h reperfusion. Rats were orally given different doses of n-butyl alcohol extracts (NBES) of RPP or saline for one week before induction of ischemia. Neurological defect scoring, cerebral infarct volume, oxidative stress markers, inflammatory reaction and nerve cell apoptosis were then estimated.
It showed that NBES could alleviate in a dose-dependent manner neurological deficit and reduce the infarct volume in vivo. The protective effects of NBES were associated with increased Superoxide dismutase (SOD) activity and decreased malonaldehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels. In addition, ischemia-induced neuron apoptosis was inhibited by NBES pretreatment, and western blot showed NBES upregulated expressions of B-cell leukemia-2 (Bcl-2) and downregulated Bcl-2-associated X (Bax) expression.
NBES prevent cerebral I/R injury by alleviating neuronal oxidative injury, inflammatory reaction and neuron apoptosis. The research for the traditional use of RPP provided certain theoretical basis.