Ginsenoside Rd Protects Against Cerebral Ischemia-Reperfusion Injury Via Decreasing the Expression of the NMDA Receptor 2B Subunit and its Phosphorylated Product.

Abstract

Ginsenoside Rd (GSRd) is one of the active ingredients in ginseng. Recent studies have shown that GSRd can protect against cerebral ischemia through several pathways, one of which is mediated by the N-methyl-D-aspartate receptor (NMDAR). In this study, we aimed to investigate the effects of GSRd on the phosphorylation of the NMDAR 2B subunit (NR2B subunit) in cerebral ischemia. Ischemia-reperfusion injury (IRI) models induced by transient middle cerebral artery occlusion (MCAO) and oxygen glucose deprivation (OGD) were used to mimic in vivo or in vitro injury during cerebral ischemia. The models were pretreated or post-treated with GSRd after MCAO or OGD. As a vehicle control, 1,3-propanediol was used. The expression levels of the NR2B subunit and the phosphorylated NR2B subunit were determined using western blotting. GSRd significantly improved the behavior score, infarct volume, and viability of the cultured neurons after ischemia. GSRd inhibited the hyperphosphorylation of NR2B subunit and decreased the expression levels of NR2B subunit in cell membrane but did not change their levels in the total proteins after IRI. GSRd protected Sprague-Dawley rats and cultured neurons from IRI via inhibiting the hyperphosphorylation of NR2B subunit and decreasing its expression levels in cell membrane.