Ginsenoside?Rg1 exerts a protective effect against Aβ25-35-induced toxicity in primary cultured rat?cortical neurons through the NF-κB/NO pathway

摘要

Ginsenoside Rg1?(Rg1) is a multipotent triterpene saponin extracted from ginseng, and has been proven to act as a nootropic agent against various types of neurological damage. The present study was designed to investigate the neuroprotective effect and the underlying mechanisms of Rg1 on apoptosis induced by β-amyloid peptide?25-35?(Aβ25-35) in primary cultured cortical neurons. The primary neurons were preincubated with 20?μM Rg1 for 24?h and exposed to 10?μM Aβ25-35 for 72?h. In the present study, we found that Rg1 prevented nuclear factor κ-light-chain?enhancer of activated B?cells (NF-κB) nuclear translocation and IκB-α phosphorylation in primary cultured cortical neurons after Aβ25-35 exposure by scavenging excess reactive oxygen species?(ROS); ROS was measured using DCFDA and examined using a fluorescence microscope. In addition, Rg1 successfully suppressed Aβ25?35-inducible nitric oxide synthase?(iNOS) expression and nitric oxide?(NO) production in a NF-κB-dependent manner; the suppression of NO was clearly illustrated by the NO production assay. Pretreatment of the cells with Rg1 elevated the proportion of Bcl-2/Bax, lessened the release of cytochrome?c from mitochondria into cytoplasm and then blocked mitochondrial apoptotic cascades after Aβ25-35 insult by lowering NO generation. Taken together, our data demonstrate that Rg1 rescues primary cultured cortical neurons from Aβ25-35-induced cell apoptosis through the downregulation of the NF-κB/NO signaling pathway.