选择性代谢性谷氨酸受体5激动剂CHPG对创伤性神经元损伤的保护作用研究  

Neuroprotective Effects of the Selective mGluR5 Agonist CHPG Against Traumatic Neuronal Injury

作　　者：陈继军[1] 李随芬 李超[1] 赵鹏[1] 尹文[1] 

机构地区：[1]第四军医大学西京医院急诊科,陕西西安710032 [2]陕西泾阳县医院,陕西泾阳713700

出　　处：《现代生物医学进展》2011年第24期4808-4810,共3页Progress in Modern Biomedicine

基　　金：国家自然科学基金资助项目(81070063)

摘　　要：目的:研究选择性代谢性谷氨酸受体5激动剂2-氯-4羟苯基甘氨酸(CHPG)对创伤性神经元损伤的保护作用,并初步探讨其保护机制。方法:大鼠皮层神经元原代培养10天后,采用机械划伤的方法建立损伤模型,采用乳酸脱氢酶(LDH)测定和Hoechst 33342染色观察CHPG对神经元的保护作用。结果:①CHPG显著降低损伤后LDH的释放和神经元凋亡。②与对照组相比,CHPG增加了ERK与Akt的磷酸化水平。③使用ERK抑制剂PD98059或者Akt抑制剂LY294002都可以部分逆转CHPG的保护作用。结论:CHPG可以减轻创伤性神经元损伤,这种保护作用可能是由ERK和Akt信号通路介导的。Objective： To investigate the neuroprotective effects of the selective mGluR5 agonist（R,S）-2-chloro-5-hydrox-yphenylglycine（CHPG） on traumatic neuronal injury and to investigate the possible mechanism.Methods： After cultured for 10 days,rat cortical neurons were injured by mechanical scratch and lactate dehydrogenase（LDH） release.Hoechst 33342 staining was used to detect the protective effects of CHPG.Results： ① CHPG can significantly attenuate LDH release and neuronal apoptosis after traumatic injury.② Compared with that in the control group,the phosphorylation levels of ERK and Akt increased in the presence of CHPG.③ ERK in-hibitor PD98059 or Akt inhibitor LY294002 can partially reversed the CHPG＇s neuroprotective effects.Conclusion： CHPG attenuates neuronal damage induced by traumatic injury,and the protective effects are possibly mediated by activation of ERK and Akt signaling pathway.

关 键 词：凋亡 神经保护作用 ERK AKT 

分 类 号：Q95-3[生物学—动物学] R446.1[医药卫生—诊断学]