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。 Objective To investigate the effect of tea polyphenols on the damage of lens of rats induced by D-galactose and its mechanism. Methods D-galactose (400 mg/kg bw) was injected intraperitoneally. After 2 weeks, model rats were given aminoguanidine (75 mg/kg bw) and tea polyphenols were high, medium and low (150, 75, 37.5 mg/kg bw). ) Dose treatment until the 14th. The animals were treated and blood was taken to determine red cell aldose reductase (AR) activity, glycated hemoglobin, serum fructosamine (FRA), and advanced plasma glycation end products (AGEs) content; the eye lens was taken to determine AR, GR, SOD, and SDH Activity, determination of AGEs, GSH, MDA content and lactate dehydrogenase (LDH) leakage, flow cytometry to detect the apoptosis of lens epithelial cells, transmission electron microscopy observed changes in ultrastructure of lens epithelial cells. Results After 14-day treatment of animals with D-galactose, the levels of glycosylated hemoglobin, serum fructosamine, AGEs, and AR activity were significantly increased. Accompanied by the increase of AGEs content and AR activity of the lens, the activity of antioxidant enzymes was decreased, and the oxidation products were increased. Apoptosis and nuclear and mitochondrial structural damage appear in lens epithelial cells. After 12 weeks of tea polyphenols treatment, the activities of red blood cells and crystal AR in animals were significantly reduced, the levels of glycosylated hemoglobin, serum fructosamine and AGEs were reduced, the content of AGEs, MDA, and release of LDH were decreased, and the activities of GR, SDH, and SOD were increased, and the lens was decreased. The rate of apoptosis in epithelial cells reduces the extent of nuclear and mitochondrial structural damage. Conclusion D-galactose can induce glycosylation and oxidative stress damage of the lens and the eye of rats, leading to changes in the nucleus and mitochondrion structure of the lens and induction of apoptosis. Tea polyphenols may inhibit glycosylation and oxidative stress. Reacts and provides protection against damage.