论文部分内容阅读
雄性Wistar大鼠40只,随机平均分为4组,正常对照组、糖尿病组、糖尿病依帕司他(10mg/kg/d)治疗组、糖尿病川芎嗪(100mg/kg/d)治疗组,腹腔注射链脲佐菌素(65mg/kg)诱发糖尿病。16周后,处死大鼠,分离晶体,测定组织AR活性,观察视网膜Bcl-2、Bax的表达。结果:1.与正常对照组相比,糖尿病组AR活性明显升高(P<0.001),依帕司他治疗组、川芎嗪治疗组AR活性较糖尿病组明显降低(P<0.01),而血糖无明显变化。2.糖尿病组视网膜Bcl-2、Bax蛋白表达明显增加,依帕司他治疗组、川芎嗪治疗组的Bcl-2、Bax蛋白表达较糖尿病组明显减少。结论:1.AR过度激活通过促进Bcl-2、Bax蛋白的表达诱导细胞凋亡,而参与DR的发生与发展。2.ARts通过抑制醛糖还原酶活性,调节Bax、Bcl-2的表达抑制细胞凋亡,延缓DR的发展。3.川芎嗪对AR抑制作用与典型ARIs依帕司他相似,且价格低、副作用少,值得临床推荐应用。
40 male Wistar rats were randomly divided into 4 groups: normal control group, diabetic group, diabetic Epalrestat (10mg/kg/d) treatment group, diabetic Ligustrazine (100mg/kg/d) treatment group, abdominal cavity Diabetes was induced by streptozotocin (65 mg/kg) injection. After 16 weeks, the rats were killed and the crystals were separated. The activity of tissue AR was measured and the expression of Bcl-2 and Bax in the retina was observed. Results: 1. Compared with the normal control group, the AR activity in the diabetic group was significantly higher (P<0.001), and the AR activity in the epalrestat treatment group and the tetramethylpyrazine treatment group was significantly lower than that in the diabetic group (P<0.01). No significant changes. 2. The expression of Bcl-2 and Bax in the retina was significantly increased in the diabetic group. The expression of Bcl-2 and Bax in the epalrestat-treated group and the tetramethylpyrazine-treated group was significantly decreased compared with the diabetic group. Conclusion:1. Over-activation of AR induces apoptosis through promoting the expression of Bcl-2 and Bax proteins, and participates in the occurrence and development of DR. 2.ARts inhibit aldose reductase activity and regulate the expression of Bax and Bcl-2 to inhibit apoptosis and delay the development of DR. The inhibitory effect of tetramethylpyrazine on AR is similar to that of typical ARIs. Its low price and few side effects are worthy of clinical application.