茶多酚对D-半乳糖诱致大鼠眼晶状体损伤的干预作用及其机制

目的探讨茶多酚对D-半乳糖诱致大鼠眼晶体损伤的干预作用及其机制。方法D-半乳糖(400mg/kg bw)腹腔注射给药,2w后模型大鼠同时给予氨基胍(75mg/kg bw)和茶多酚高、中、低(150、75、37.5mg/kg bw)剂量处理至第14w。处理动物并取血测定红细胞醛糖还原酶(AR)活性、糖化血红蛋白、血清果糖胺(FRA)和晚期血浆糖基化终末产物(AGEs)含量;取眼晶状体测定AR、GR、SOD和SDH活性,测定AGEs、GSH、MDA含量和乳酸脱氢酶(LDH)漏出量,流式细胞术检测晶状体上皮细胞凋亡情况,透射电镜观察晶状体上皮细胞超微结构的变化。结果D-半乳糖处理动物14w后,体内糖化血红蛋白、血清果糖胺、AGEs水平和AR活性明显升高,并伴有眼晶状体AGEs含量和AR活性的增加,抗氧化酶活性降低,氧化产物增加,晶状体上皮细胞出现凋亡及细胞核和线粒体结构的损伤。茶多酚处理12w后,明显降低动物体内红细胞和晶体AR活性,降低糖化血红蛋白、血清果糖胺和AGEs含量,降低晶状体AGEs、MDA含量和LDH释放量,提高GR、SDH和SOD活性,并降低晶状体上皮细胞凋亡率,减少细胞核和线粒体结构损伤的程度。结论D-半乳糖可诱致大鼠全身和眼晶状体糖基化和氧化应激性损伤,导致眼晶体细胞核和线粒体结构改变,诱导细胞凋亡,茶多酚可能通过抑制糖基化和氧化应激反应,对其损伤提供保护作用。

THE INTERVENTION EFFECTS OF TEA POLYPHENOLS ON DAMAGE OF LENS EPITHELIAL CELLS IN RATS INDUCED BY D-GALACTOSE AND ITS MECHANISM

Objective To investigate the intervention effects of tea polyphenols on lens cells damage induced by D-galactose in rats’ eyes and and its mechanism. Method D-galactose (400mg/kg bw) was injected into rats i.p. for 14 w to induce glycosylation and lens cells damage animal model, and aminoguanidine (75mg/kg bw) and tea polyphenols (150, 75, 37.5 mg/kg bw) were administered for 12 w i.g. at the 3th w. All animals were killed and blood samples were taken to measure the activity of RBC aldose reductase (AR), the level of serum fructosamine, blood glycohaemoglobin and plasma advanced glycation end-products. The lens of eyes were taken to detect the activities of AR, GR, SOD and SDH, and the amounts of AGEs, GSH, MDA or outleakage of LDH were measured respectively. The ultrastructure and apoptosis of lens epithelial cells were examined by transmission electron microscope and flow cytometer, respectively. Results Animals were treated with D-galactose for 14 w, serum fructosamine, glycohaemo-globin, AGEs, and AR activity were significantly increased. AGEs and AR activity in lens were increased,antioxidase activity was decreased and oxidative product was increased, apoptosis and damage of mitochondria and cell nucleus in lens cells appeared. After treatment of TP for 12 w, the activity of AR and the level of fructosamine, glycohaemoglobin and AGEs were significantly decreased, and the outleakage of LDH and amount of MDA were also decreased. The activities of GR, SDH and SOD were increased, and apoptotic rate of lens cells was reduced and morphology of mitochondria and cell nucleus was improved. Conclusion D-galactose can induce the damage of cell nucleus and mitochondria and apoptosis in lens cells by glycosylation and oxidative stress. Tea polyphenols can inhibit the glycosylation and oxidative stress and protect from the damage of nucleus and mitochondria in lens cells.