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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 evaluate the induced expression of heat shock protein 70 (HSP70) in rat retinal neurons (RNs) and Müller cells and its protective effect on retinal neurons damaged by low glucose and glutamate. Methods The rat HSPs and Müller cells were incubated in vitro with heat shock (42 ℃ for 1 h) and immunocytochemistry for the passage of time. The effect of low glucose (0.56 mmol / L glucose, h) and glutamic acid (10 μmol / L for 6 h), MTT assay was used to evaluate cell viability and HSP70 antibody was used to block its expression. Results Heat shock enhanced the expression of HSP70 in RNs and Müller cells. After heat shock pretreatment, the cell viability of RNs significantly increased after hypoglycemia and glutamate injury, which could be blocked by HSP70 antibody. Conclusion Heat shock can induce the high expression of HSP70 in RNs and Müller cells and enhance the tolerance of RNs to hypoglycemic and glutamate excitotoxicity.