【摘要】 目的热休克预处理诱导的热休克蛋白27对晶状体上皮细胞的保护作用,并初步探讨其机制。方法体外培养人晶状体上皮细胞株HLB3细胞,分为正常对照组、氧化损伤组和热休克处理组,观察过氧化氢(H2O2)处理后各组细胞活力、SOD、CAT的改变情况;AnnexinⅤFITC流式细胞仪检测晶状体上皮细胞凋亡;RTPCR检测各组中HSP27及p21基因的表达。结果热休克预处理可诱导HSP27产生,显著增加细胞活力0.27±0.04(与氧化损伤组0.24±0.02相比P<0.05),细胞凋亡率明显降低(8.34±1.19)%(与氧化损伤组15.69%±1.54%比较P<0.05),保护超氧化物岐化酶0.61±0.07(与氧化损伤组0.41±0.08比较P<0.05)、过氧化氢酶活性0.99±0.14(与氧化损伤组0.33±0.06相比P<0.05),降低p21mRNA的表达。结论热休克预处理可能通过诱导HSP27的表达保护氧化损伤的晶状体上皮细胞;降低p21基因表达并抑制氧化损伤后晶状体上皮细胞凋亡可能是其保护机制之一。更多还原

【Abstract】 Objective To study the mechanism and the effect of heat shock pretreatment on hydrogen peroxide induced injury of human lens epithelial cells.Methods Cultured human lens epithelial cells (HLB-3) were divided into three groups:control group,oxidation injury group and heat shock pretreatment group.Cells viability and SOD、catalase activities were analyzed.The apoptosis was evaluated with flow cytometry Annexin V Flous staining.RT-PCR was used to determine the expression of heat shock protein 27 and P21 gene in HLB-3 cells.Results Heat shock pretreatment could induce the expression of HSP 27,improve cell viability 0.27±0.04(compared with oxidative group 0.24±0.02,P<0.05),protective of the activities of SOD 0.61±0.07(compared with oxidative group 0.41±0.08,P<0.05) and catalase 0.99±0.14(compared with oxidative group 0.33±0.06,P<0.05),decrease the apoptosis ratio(8.34±1.19)%(compared with oxidative group15.69±1.54%,P<0.05)and the expression of p21 mRNA significantly.Conclusion The increased expression of HSP 27 by heat shock pretreatment could play an important role in the protection on hydrogen peroxide induced injury of human lens epithelial cells.The decreased expression of p21 gene and the inhibition of cell apoptosis may be involved in the protective mechanism.更多还原