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目的 探讨实验性糖尿病大鼠晶状体上皮细胞损伤的机理以及糖障明对糖尿病性白内障的作用机制。方法 将用链脲佐菌素造成糖尿病模型的大鼠分为用糖障明治疗组 (中药组 )、 0 5 %甲基纤维素液灌胃组 (阴性对照组 )和降糖灵混悬液灌胃组 (阳性对照组 ) ,并以与实验组同龄的正常大鼠作为正常对照组。用末端脱氧核苷酸转移酶介导生物素标记的脱氧尿嘧啶核苷三磷酸缺口末端 (TUNEL)标记技术检测晶状体上皮细胞凋亡 ,用计算机图像分析技术对所测定的面积百分比进行定量分析。结果 与正常对照组相比 ,显示窗晶状体上皮细胞TUNEL标记阳性染色率在阴性对照组明显增高 ,中药治疗组明显低于阴性对照组和阳性对照组 (P <0 0 5～ 0 0 0 1 )。结论 持续的高血糖可导致大鼠晶状体上皮细胞发生不可逆的损伤 ,糖障明能有效抑制糖尿病大鼠晶状体上皮细胞凋亡 ,从而抑制糖尿病性白内障的形成。
Objective To investigate the mechanism of lens epithelial cell injury in experimental diabetic rats and the mechanism of action of glycosylate on diabetic cataract. METHODS: Rats with diabetes mellitus model induced by streptozotocin were divided into two groups: glycoside-treated group (TCM group), 05% methylcellulose solution group (negative control group), and Jiangtangling mixture. The group (positive control group) and normal rats of the same age as the experimental group served as normal control group. Apoptosis of lens epithelial cells was detected by terminal deoxynucleotidyl transferase-mediated biotin-labeled nick endiacin (TUNEL) labeling technique, and the area percentage determined was quantitatively analyzed by computer image analysis technique. Results Compared with the normal control group, the positive staining rate of TUNEL in the lens epithelial cells was significantly higher in the negative control group, and the Chinese medicine treatment group was significantly lower than the negative control group and the positive control group (P <0 05 to 0 0 0 1). . Conclusion Continuous hyperglycemia can lead to irreversible damage to rat lens epithelial cells, and glycogen barrier can effectively inhibit apoptosis of lens epithelial cells in diabetic rats, thereby inhibiting the formation of diabetic cataract.