摘要
目的探讨酸性成纤维细胞生长因子(aFGF)对庆大霉素损伤的海马星形胶质细胞保护作用可能的机制。方法新生24 h Sprague-Dawley大鼠分离、纯化海马星形胶质细胞,胶质纤维酸性蛋白(GFAP)免疫荧光染色鉴定,传3代细胞接种于24孔培养板培养3 d,分为3组:对照组正常培养,损伤组以2.0 g/L庆大霉素培养24 h,保护组加入4.25μg/L aFGF培养24 h后再加入2.0g/L庆大霉素培养24 h。Western blotting检测P38、细胞外信号调节蛋白激酶(ERK)1、ERK2、c-Jun氨基末端激酶(JNK)1、JNK2的表达。结果成功培养细胞,纯度>95%。与对照组比较,损伤组ERK1表达增加(P<0.05);保护组与损伤组比较,P38表达增加(P<0.05),ERK1表达减少(P<0.05);其余两两比较均无显著性差异(P>0.05)。结论信号通路中的P38和ERK1可能在aFGF对抗庆大霉素诱导的海马星形胶质细胞损伤过程中发挥作用。
Objective To explore the mechanism of the protection of acidic fibroblast growth factor（aFGF） for hippocampal astrocytes from injury induced by gentamicin. Methods Hippocampal astrocytes were isolated from newborn（24 hours） Sprague- Dawley rats, purified, and identified with glial fibrillary acidic protein（GFAP） immunofluorescence. The third generations were cultured for 3 days and divided into 3 groups： control group was cultured routinely, injury group was cultured with 2.0 g/L gentamicin for 24 hours, and protection group was cultured with 4.25 μg/L aFGF for 24 hours and then cultured with 2.0 g/L gentamicin for 24 hours. Western blotting was adopted to detect the expressions of P38, extracellular signal-regulated kinase（ERK）1/2 and c-Jun N-terminal kinase（JNK）1/2. Results Hippocampal astrocytes were culturated successfully with the purity above 95%. The ERK1 increased in the injury group compared with the control group（P〈0.05）. Compared with the injury group, the p38 increased（P〈0.05） and the ERK1 decreased（P〈0.05） in the protection group. There was no significant difference among others（P〉0.05）. Conclusion The mitogen- activated protein kinase signal pathway, especially P38 and ERK1, may associate with the protection of aFGF for hippocampal astrocytes from injury induced by gentamicin.
出处
《中国康复理论与实践》
CSCD
北大核心
2016年第3期270-273,共4页
Chinese Journal of Rehabilitation Theory and Practice
基金
国家"863"计划课题(No.2004AA2Z3C60)
广西医疗卫生重点科研课题(No.2011046)
