独活香豆素对Aβ25-35损伤神经元的保护作用及机制研究  

Neuroprotective effects of total coumarins of Angelica pubescens(TCA) and mechanism against neuron damage induced by Aβ25-35

作　　者：张晓丹[1] 胡昱[1] 张囡[1] 赵丹[1] 郝海光[1] 孙东[1] 李红艳[1] 杨静娴[1] 

机构地区：[1]辽宁中医药大学药学院药理教研室,大连116600

出　　处：《中药药理与临床》2012年第5期57-61,共5页Pharmacology and Clinics of Chinese Materia Medica

基　　金：国家自然科学基金(No.81173580);辽宁省自然科学基金(201102144);沈阳市科技专项资金(F11-264-1-42)

摘　　要：目的:研究独活香豆素对β淀粉样蛋白(Aβ25-35)损伤神经元的保护作用及可能机制。方法:从新生乳鼠大脑皮层中分离纯化神经元,与Aβ25-35、不同浓度独活香豆素和丹酚酸B共同孵育24 h,用噻唑蓝(MTT)法和乳酸脱氢酶(LDH)测定法检测细胞存活率与LDH释放量,用Hoechst 33258染色检测Aβ25-35诱导的神经元凋亡,用RT-PCR法检测凋亡相关基因Bcl-2、Caspase-3 mRNA的表达量。结果:独活香豆素(10、50、100、150μg/ml)能明显提高Aβ25-35(30μM)损伤神经元的存活率,降低LDH释放量,抑制神经元凋亡,以浓度为100μg/ml时作用最显著,作用强度与丹酚酸B相当;独活香豆素能提高神经元Bcl-2 mR-NA、降低Caspase-3 mRNA的表达量。结论:独活香豆素对Aβ25-35损伤神经元具有保护作用,其机制可能与抑制促凋亡基因Caspase-3、促进抗凋亡基因Bcl-2 mRNA表达有关。Objective：To investigate the neuroprotective effects and mechanism of total coumarins of Angelica pubescens Maxim（TCA） against Aβ25-35 induced neuron damage.Methods：Primary neurons were isolated and purified from cerebral cortex of suckling mouse.The neurons were co-cultured with Aβ25-35,TCA or Salvianolic acid B for 24 h,then cell viability,LDH release and apoptosis were detected by MTT,LDH assays and Hoechst 33258 staining;Bcl-2 and Caspase-3 mRNA expressions were detected by RT-PCR.Results：TCA（10、50、100、150 μg/ml） increased cell viability,decreased LDH release and inhibited neuron apoptosis induced by Aβ25-35（30 μM）,especially at 100 μg/ml,the neuroprotective efficiency is similar to that of Salvianolic acid B;TCA increased Bcl-2 and decreased Caspase-3 mRNA expression.Conclusions：TCA possesses the neuroprotective effects on Aβ25-35-damaged neuron,which may be associated with induction of a pro-apoptotic gene Bcl-2 and inhibition of an anti-apoptotic gene Caspase-3 mRNA expression in neurons.

关 键 词：独活香豆素 神经元 AΒ25-35 凋亡 

分 类 号：R285[医药卫生—中药学]