中南大学学报(医学版)
中南大學學報(醫學版)
중남대학학보(의학판)
JOURNAL OF CENTRAL SOUTH UNIVERSITY（MEDICAL SCIENCES）
2011年
1期
21-26
,共6页
汤轶波%张玮%唐卉凌%李澎涛
湯軼波%張瑋%唐卉凌%李澎濤
탕질파%장위%당훼릉%리팽도
胰岛素样生长因子-1%神经元%信号通路%氧糖剥夺模型
胰島素樣生長因子-1%神經元%信號通路%氧糖剝奪模型
이도소양생장인자-1%신경원%신호통로%양당박탈모형
insulin like growth factor 1%neuron%signal pathway%oxygen and glucose deprivation model
目的:观察胰岛素样生长因子-1( insulin like growth factor 1, IGF-1)对缺氧缺糖神经元的保护作用并探讨其可能的作用机制.方法:构建体外培养的神经元氧糖剥夺模型(oxygen and glucose deprivation, OGD),第7天将培养的神经元分为8组(4组暴露于氧糖剥夺,另4组非暴露),分别施加纯化的IGF-1单体,并观察加入PI3K和MAPK信号通路的特异性阻断剂LY294002和PD98059的效应,利用MTT法分别观察各组神经元的细胞活性;Western印迹观测不同干预因素下Akt 和 p-Akt蛋白的表达情况.结果:神经元正常组和缺血缺氧模型组,加入IGF-1后细胞增殖活性均显著升高 (P＜0.05);而同时加入IGF-1和LY294002后,IGF-1促神经元活性的作用被明显抑制 (P＜0.05),反之同时加入IGF-1与PD98059后,IGF-1发挥促神经元存活的作用未被明显阻滞 (P＞0.05).Western印迹结果示IGF-1可显著上调p-Akt的表达,这种上调作用可以被LY294002阻滞.结论:IGF-1有明确的神经保护作用,其可能是通过PI3K/Akt通路来发挥作用的.
目的:觀察胰島素樣生長因子-1( insulin like growth factor 1, IGF-1)對缺氧缺糖神經元的保護作用併探討其可能的作用機製.方法:構建體外培養的神經元氧糖剝奪模型(oxygen and glucose deprivation, OGD),第7天將培養的神經元分為8組(4組暴露于氧糖剝奪,另4組非暴露),分彆施加純化的IGF-1單體,併觀察加入PI3K和MAPK信號通路的特異性阻斷劑LY294002和PD98059的效應,利用MTT法分彆觀察各組神經元的細胞活性;Western印跡觀測不同榦預因素下Akt 和 p-Akt蛋白的錶達情況.結果:神經元正常組和缺血缺氧模型組,加入IGF-1後細胞增殖活性均顯著升高 (P＜0.05);而同時加入IGF-1和LY294002後,IGF-1促神經元活性的作用被明顯抑製 (P＜0.05),反之同時加入IGF-1與PD98059後,IGF-1髮揮促神經元存活的作用未被明顯阻滯 (P＞0.05).Western印跡結果示IGF-1可顯著上調p-Akt的錶達,這種上調作用可以被LY294002阻滯.結論:IGF-1有明確的神經保護作用,其可能是通過PI3K/Akt通路來髮揮作用的.
목적:관찰이도소양생장인자-1( insulin like growth factor 1, IGF-1)대결양결당신경원적보호작용병탐토기가능적작용궤제.방법:구건체외배양적신경원양당박탈모형(oxygen and glucose deprivation, OGD),제7천장배양적신경원분위8조(4조폭로우양당박탈,령4조비폭로),분별시가순화적IGF-1단체,병관찰가입PI3K화MAPK신호통로적특이성조단제LY294002화PD98059적효응,이용MTT법분별관찰각조신경원적세포활성;Western인적관측불동간예인소하Akt 화 p-Akt단백적표체정황.결과:신경원정상조화결혈결양모형조,가입IGF-1후세포증식활성균현저승고 (P＜0.05);이동시가입IGF-1화LY294002후,IGF-1촉신경원활성적작용피명현억제 (P＜0.05),반지동시가입IGF-1여PD98059후,IGF-1발휘촉신경원존활적작용미피명현조체 (P＞0.05).Western인적결과시IGF-1가현저상조p-Akt적표체,저충상조작용가이피LY294002조체.결론:IGF-1유명학적신경보호작용,기가능시통과PI3K/Akt통로래발휘작용적.
Objective To investigate the protective effects of insulin like growth factor 1(IGF-1) on cortical neurons under condition of hypoxia and the possible mechanism. Methods Cerebral cortical neurons from newborn rats were cultured under the condition of oxygen and glucose deprivation (OGD) . On day 7, neurons were treated with IGF-1 or IGF-1 plus LY294002 or PD98059 under condition of OGD or normal condition. MTT assay was used to analyze the viability of neurons in each group. The expression of total Akt and p-Akt were analyzed by Western blot. Results Compared with the control, the neuron viability was significantly higher in IGF-1 treated group under normal or OGD condition (P＜0.05). The protective effects of IGF-1 were attenuated in the presence of LY294002 but not PD98059. The result of Western blot showed IGF-1 upregulated the expression of p-Akt, which was inhibited by LY294002. Conclusion PI3K pathway may play an important role in neuroprotection afforded by IGF-1.
