NEUROPROTECTIVE ROLE OF BAVACHIN IN A RAT MIDDLE CEREBRAL ARTERY OCCLUSION STROKE MODEL

Bavachin is a flavonoid isolated from the seeds of Psoralea corylifolia. Studies have shown that bavachin inhibits neuroinflammation and oxidative stress. However, its protective effects in ischemic stroke remain unclear. In this study, we investigated the therapeutic potential of bavachin and its underlying mechanisms in a rat middle cerebral artery occlusion (MCAO) stroke model. Adult male Sprague Dawley (SD) rats underwent right-sided MCAO for 90 minutes and received intraperitoneal injection of bavachin at 40 mg/kg for 3 consecutive days, with the first dose administered 3 hours before MCAO onset, and the remaining doses administered at 24 and 48 hours after MCAO. Body weight and a modified Neurological Severity Score (mNSS) were assessed daily before and after MCAO until sacrifice at 72 hours, when infarct volume and cerebral edema index were determined. The inhibitor of nuclear factor kappa B alpha (IkappaB alpha), p65 and their phosphorylated forms, peroxisome proliferator-activated receptor gamma (PPAR-gamma) were investigated in the ipsilateral cortex using western blot. Bavachin significantly reduced the mNSS and infarct volume at 72 hours. Additionally, bavachin did not affect body weight and cerebral edema index. Compared to the MCAO group, bavachin treatment significantly inhibited the p-p65/p65 and the expression of PPAR-gamma. However, bavachin had no significant effect on p-IkappaB alpha/IkappaB alpha. This study indicates that bavachin plays a neuroprotective role in a rat MCAO stroke model. The underlying mechanisms are associated with the inhibition of p-p65/p65 and PPAR-gamma expression. These results imply the potential of bavachin as a therapeutic agent for ischemic stroke.