Dynamic Study Of HSP70 Expression And Proliferation, Apoptosis In The Lens Epithelial Cells Of Streptozotocin-diabetic Rats

Objective To investigate the expression of the HSP70, proliferation and apoptosis in the lens epithelial cells (LECs) of streptozotocin(STZ)-diabetic rats, and to evaluate the role of heat shock protein 70 (HSP70), proliferation and apoptosis in the pathogenesis of diabetic cataract.Methods 120 SD rats were randomly divided into two groups: normal control and cataract. Diabetic cataract was induced by STZ intraperitoneal injection(70mg/kg in 0.1 mol/L sodium citrate buffer). Lens were examined using a slitlamp once a week. At the end of 2 weeks, 4 weeks, 8 weeks after STZ injection, eyeballs were isolated. Terminal deoxynucleotidyl transferase梞ediated dUTP biotin nick end labeling (TUNEL) was used to analyzed the lens epithelial cells(LECs) apoptosis , and immunohistochemical streptavidin-peroxidases ( S-P ) method to detect the expression of HSP70, proliferating cell nuclear antigen (PCNA) in normal and diabetic LECs. Results1.The lens of control group were always completely transparent throughout the period of experiment, and the lens of cataract group began to exhibited vacuolar stage by week 2 and floccule by week 4 , and nearly opacity by week 8.2. The expression of HSP70 , PCNA and LECs apoptosis were significantly different between normal and diabelic LECs (P<0.01) . During the progression of cataract, the expression of HSP70 and PCNA graduallyincreased, and LECs apoptosis decreased (P<0. 05) .3. During the progression of cataract, the expression of HSP70 was positively correlated with that of PCNA (P<0. 01) , but was negatively correlated with the LECs apoptosis (P<0. 01) .Conclusions Proliferation and apoptosis of LECs were ubiquity during the progression of cataract, and were significantly correlated with the development of diabetic cataract. The expression of HSP70 continually increased , which played a critical role in the pathogenesis of diabetic cataract. It caught LECs proliferate, then migrate, fibrosis, and leaded to subcapsule opacity, but on the other hand it inhibited the progress of the LECs apoptosis, thus protected diabetic lens from opacity.