论文部分内容阅读
背景:肾衰泻浊汤临床治疗以泻浊解毒、补益脾肾为主。目的:观察肾衰泻浊汤对慢性肾衰竭模型大鼠肾脏局部血管内皮细胞损伤的保护和对血管内皮生长因子受体表达的调控作用。方法:将60只Wistar大鼠随机分为正常对照组、模型组、中药低剂量组、中药中剂量组、中药高剂量组、氯沙坦钾组,后5组以腺嘌呤诱导建立慢性肾衰竭动物模型,中药低、中、高剂量组分别灌胃给予6,12,24g/(kg·d)肾衰泻浊汤,氯沙坦钾组给予氯沙坦钾。结果与结论:与模型组比较,各治疗组大鼠血肌酐、尿素氮及血β2-微球蛋白、尿微量白蛋白、血清可溶性细胞间黏附因子1、血管内皮生长因子、因子Ⅷ相关抗原、肾脏指数显著减少(P<0.05),且血β2-微球蛋白、尿微量白蛋白与血肌酐、尿素氮呈显著正相关性。各治疗组大鼠肾组织损伤明显减轻,以中药中剂量组、氯沙坦钾组损伤最轻。表明肾衰泻浊汤能降低慢性肾衰竭大鼠血肌酐、尿素氮及血β2-微球蛋白、尿微量白蛋白水平,延缓慢性肾衰进展,其作用机制可能与调节可溶性细胞间黏附因子1、血管内皮生长因子、因子Ⅷ相关抗原有关。
Background: The clinical treatment of Shenyin Xiezhuo Decoction detoxification, replenishing spleen and kidney-based. Objective: To observe the effect of Shenshuai Xiezhuo decoction on renal local vascular endothelial cell injury and the regulation of vascular endothelial growth factor receptor expression in chronic renal failure model rats. Methods: Sixty Wistar rats were randomly divided into normal control group, model group, low dose Chinese medicine group, middle dose Chinese medicine group, high dose Chinese medicine group and losartan potassium group. The latter five groups were induced by adenine to establish chronic renal failure Animal models and low, medium and high dose groups of Chinese medicine were given intragastric administration of 6, 12, 24g / (kg · d) of renal failure diarrhea soup, Losartan potassium group given losartan potassium. RESULTS AND CONCLUSION: Compared with model group, serum creatinine, blood urea nitrogen, blood β2-microglobulin, urinary albumin, serum soluble intercellular adhesion molecule 1, vascular endothelial growth factor, factor Ⅷ related antigen, Kidney index decreased significantly (P <0.05), and blood β2-microglobulin, urinary albumin and serum creatinine, urea nitrogen was positively correlated. The renal tissue injury of rats in each treatment group was significantly reduced, and the lightest was the middle-dose group and losartan potassium group. The results showed that JRF can reduce serum creatinine, blood urea nitrogen, blood β2-microglobulin and urine microalbuminuria in chronic renal failure rats and delay the progression of chronic renal failure. The mechanism may be related to the regulation of soluble intercellular adhesion molecule 1 , Vascular endothelial growth factor, factor Ⅷ related antigen.