热休克蛋白70在视网膜神经元和Müller细胞中的诱导及其保护作用  

Expression and protective effect of induced heat shock protein 70 in retinal neurons and Müller cells

作　　者：白海青[1] 王竫华[1] 王大博[1] 李树宁[1] 张蕊石[1] 

机构地区：[1]青岛大学医学院附属医院眼科

出　　处：《中华眼底病杂志》2005年第2期110-113,共4页Chinese Journal of Ocular Fundus Diseases

摘　　要：目的　评价大鼠视网膜神经元 (RNs)和 Müller细胞中热休克蛋白 (HSP) 70的诱导表达 ,及其对低糖和谷氨酸损伤的视网膜神经元的保护作用。　方法　大鼠 RNs和 Müller细胞体外培养体系分别经过热休克处理 (42℃下 1h)及免疫细胞化学法检测 HSP70表达的时间经过 ;并对 RNs进行低糖(0 .5 6 mmol/ L葡萄糖 ,作用 6 h)和谷氨酸 (10 0 μmol/ L,作用 6 h)兴奋毒性损伤 ,四唑盐 (MTT)比色法评价细胞存活能力 ,同时用 HSP70抗体阻断其表达。　结果　热休克后大鼠 RNs和 Müller细胞中 HSP70高效表达 ;经热休克预处理 ,RNs在低糖和谷氨酸盐损伤后的细胞活力明显提高 ,该现象可被 HSP70抗体阻断。　结论　热休克能够诱导 RNs和 Müller细胞高效表达 HSP70 ,从而增强 RNs对低糖和谷氨酸兴奋毒性损伤的耐受能力。Objective To investigate the expression of induced heat shock protein (HSP) 70 in rat′s retinal neurons (RNs) and Müller cells, and evaluate the protective effect of HSP 70 on RNs injured with glucose deprivation and glutamate. Methods Rat′s RNs and Müller cells cultured in vitro were treated with heat shock (42℃ for 1 hour), and duration of the expression of HSP70 was detected by immunocytochemical techniques. Viability of the cells was measured by methyl thiazolyl tetrazolium (MTT) chromatometry after incitant toxic injury with glucose deprivation (0.56 mmol/L glucose for 6 hours) and glutamate (100 μmol/L for 6 hours). Simultaneously, the expression was interdicted by HSP70. Results Hypereffective expression of HSP70 was found in cultured RNs and Müller cells after heat shock. The viability of RNs pretreated by heat shock after injured with glucose deprivation and glutamate significantly increased which could be interdicted by HSP70 antibody. Conclusion Hypereffective expression of HSP 70 may be induced by heat shock, which enhances the ability of tolerance of RNs to the incitant toxic injury by glucose deprivation and exitotoxicity.

关 键 词：视网膜神经元 HSP70 保护作用 细胞 大鼠 损伤 兴奋毒性 结论 能力 体系 

分 类 号：R774[医药卫生—眼科]