Neuroprotection of ginsenoside Rgl on Aβ 25-35-induced toxicity in primary cultured rat cortical neurons via NF-κB/NO pathway
作者单位：Department of PharmacyThe First Affiliated HospitalCollege of MedicineZhejiang University Division of Cardio-Cerebral Vascular and Hepatic PharmacologyCollege of Pharmaceutical SciencesZhejiang University
会议名称：《2015年浙江省医学会临床药学分会、浙江省中西医结合学会中药分会学术会议》
会议日期：2015年
学科分类：1008[医学-中药学(可授医学、理学学位)] 1006[医学-中西医结合] 100602[医学-中西医结合临床] 10[医学]
基 金：supported by National Natural Sciences Foundation of China(No 81402907) Zhejiang Provincial Natural Science Foundation of China(No LQ14H310002) Zhejiang Medical Technology Program(201474924)
关 键 词：Ginsenoside-Rg1 Aβ neuroprotection NF-κB iNOS apoptosis
摘 要：Ginsenoside Rg1(Rg1) is a multipotent triterpene saponins extracted from the traditional Chinese medicine ginseng,and has been proven to be a nootropic agent against diverse neurological *** current study was designed to investigate the neuroprotective effect and the underlying mechanisms of Rg1 on apoptosis induced by β-amyloid peptide 25-35(A β 25-35) in the primary cultured cortical *** primary neurons were preincubated with 20 μM Rg1 for 24 h and exposed to 10 μM A β 25-35 for 72 *** this study,we found that Rg1 prevented the NF- κB nuclear translocation and the I κ B- α phosphorylation in primary cultured cortical neurons after A β 25-35 exposure by scavenging excess *** addition,Rg1 successfully suppressed A β 25-35-induced iNOS expression and NO production in a NF-κB-dependent *** of Rg1 elevated the proportion of Bcl-2/Bax,lessened the release of cytochrome c from mitochondria into cytoplasm and then interdicted mitochondrial apoptotic cascades after A β 25-35 insult by lowering NO *** together,our data demonstrate that Rg1 may rescue primary cultured cortical neurons from Aβ 25-35-caused cell apoptosis via down-regulating NF-κB/NO signaling pathway.