目的:通过观察黄连素对2型糖尿病大鼠血管内皮功能的影响,探讨黄连素对2型糖尿病血管并发症的防治意义及其机制。方法:采用小剂量链脲佐菌腹腔注射加高脂饲料喂养的方法建立2型糖尿病大鼠模型,将模型动物随机分为模型组及黄连素治疗组,另设正常对照组以及正常黄连素组。药物干预治疗8周后,处理动物,检测各组动物血清中空腹血糖(FBG)、总胆固醇(TC)、甘油三酯(TG)及空腹血清胰岛素(FINS)的水平;通过离体实验方法观察离体胸主动脉条的张力反应;HE染色观察胸主动脉形态学改变。结果:与模型组比较,黄连素治疗组大鼠FBG、TC及TG水平明显下降,胰岛素敏感指数(ISI)升高(P〈0.05);黄连素治疗组大鼠乙酰胆碱(ACh)引起的内皮依赖性血管舒张反应明显改善,而硝普钠(SNP)诱导的内皮非依赖性舒张反应各组间比较差异无显著性(P〉0.05);黄连素治疗组大鼠糖尿病引起的血管内皮病变明显减轻;与正常对照组比较,正常大鼠给予黄连素灌胃,上述指标未出现明显改变。结论:黄连素对2型糖尿病早期出现的血管内皮损伤有良好的保护作用,机制可能与其降血糖、调节血脂、改善胰岛素抵抗及内皮依赖性的血管舒张反应等作用有关。
Objective To investigate the effects of berberine on vascular endothelial function in type 2diabetic rats and explore the prophylactic and therapeutic significance and pharmacological mechanism of berberine in type 2 diabetic vascular complications.Methods Wistar rats were randomly divided into four groups:diabetic group, control group,diabetic rats treated with berberine(100mg·kg-1)group,and control rats treated with berberine group.The serum fasting blood glucose(FBG),insulin,total cholesterol(TC),triglyceride(TG)and fasting insulin (FINS)levels were tested.Acetylcholine(ACh)-induced endothelium-dependent relaxation and sodium nitroprusside-induced endothelium-independent relaxation were measured in aortas for estimating endothelial function.In addition,the histopathology measurement was performed with hematoxylin and eosin staining. Results Compared with diabetic group,the FBG,TC and TG levels in diabetic rats treated with berberine were significantly decreased,meanwhile the insulin sensitivity index (ISI)was increased.The Ach-induced endothelium-dependent relaxation in the aorta from diabetic rats was significantly improved in berberine treatment group,while sodium nitroprusside(SNP)-induced endothelium-independent relaxation showed no difference among four groups. The histopathological results showed that berberine attenuated the damage of the aortic endothelium in diabetic rats. However there was no difference in these indexes between control group and berberine treated control group. Conclusion Berberine restores diabetic endothelial dysfunction through decreasing the FBS and blood lipid, improving insulin resistant and enhancing NO bioavailability.