Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model

Stroke remains a worldwide health problem.Salvianolate exerts a protective effect in various microcirculatory disturbance-related diseases,but studies of the mechanisms underlying its protective action have mainly focused on the myocardium,whereas little research has been carried out in brain tissue following ischemia-reperfusion.We assessed the neuroprotective effects of salvianolate in a rat model of cerebral ischemia-reperfusion injury induced using the suture method At onset and 24 and 48 hours after reperfusion,rats were intraperitoneally injected with salvianolate(18 mg/kg)or saline.Neurological deficit scores at 72 hours showed that the neurological functions of rats that had received salvianolate were significantly better than those of the rats that had received saline.2,3,5-Triphenyltetrazolium chloride was used to stain cerebral tissue to determine the extent of the infarct area.A significantly smaller infarct area and a significantly lower number of apoptotic cells were observed after treatment with salvianolate compared with the saline treatment Expression of heat shock protein 22 and phosphorylated protein kinase B in ischemic brain tissue was significantly greater in rats treated with salvianolate compared with rats treated with saline.Ou findings suggest that salvianolate provides neuroprotective effects against cerebra ischemia-reperfusion injury by upregulating heat shock protein 22 and phosphorylated protein kinase B expression.