Neuroprotective effects of salidroside on GSK-3β in rats with cerebral ischemia/reperfusion / 中国药理学通报

ABSTRACT

Aim To study the effects of salidroside on the caspase-9, GSK-30, NMDAR1, GluR2 in MCAO ratsand to further explore the mechanism of neuroprotection of salidroside. Methods For the first part, 36 healthy male Sprague-Dawley rats were randomly divided into sham operation (Sham) group, model (MCAO) group, and salidroside (MCAO + Sal) group. Rats were administered salidroside, or vehicle, daily for 1 day, after middle cerebral artery occlusion (MCAO) 2 h and reperfusion 1 h. The protein expression of GSK-3β, NMDAR1, GluR2 and caspase-9 was detected by Western blot. For the second part, rats were randomly divided into Sham group, SB216763 + Shamgroup, MCAO group, SB216763 + MCAO group, MCAO + Sal group, and SB216763 + MCAO + Sal group. After 30 minutes of injection of GSK-3βinhibitor SB216763 or artificial cerebrospinal fluid into the lateral ventricle, the other groups were subjected to MCAO modeling except for the sham operation group. After the modeling, the administration group was given salidroside, and the material was taken after 1 day. The protein expression of GSK-3β, NMDAR1, GluR2 andcaspase-9 was detected by Western blot. Results Compared with MCAO group, salidroside could reduce the protein expression of cleaved caspase-9 protein in mitochondria and promote the expression of pGSK-3β, NMDAR1, GluR2 protein after 1 day salidroside treatment. And the treatment of salidroside and GSK-3β inhibitor did not show remarkable additive effects. Conclusions Salidroside has a neuroprotective effect on MCAO rats, mainly by promoting GSK-3β phosphorylation, thereby inhibiting caspase-9 and promoting protein expression of NMDAR1 and GluR2.