肾衰泻浊汤对肾衰竭大鼠内皮细胞损伤的保护

Protective effect of Shenshuai Xiezhuo decoction on endothelial cells damage in rats

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 by Shenshuai Xiezhuo decoction is mainly depending on eliminate turbid fluid and remove toxic and invigorating spleen and kidney.OBJECTIVE： To investigate the protective effects of Shenshuai Xiezhuo decoction on endothelial cells damage of chronic renal failure （CRF） rats and the regulation effect on the expression of vascular endothelial growth factor （VEGF） receptor. METHODS： Sixty Wistar rats were randomly divided into control group, model group, low-dose group, middle-dose group, high-dose group and Cozaar group. The rats in the last five groups were used to establish the CRF model induced by adenine induction; rats in the low-dose group, middle-dose group and high-dose group were gavaged with 6, 12 and 24 g/（kg·d） Shenshuai Xiezhuo decoction; rats in the Iosartan potassium group were injected with Iosartan potassium.RESULTS AND CONCLUSION： Compared with the model group, the content of serum creatinine （SCr）, blood urea nitrogen, {32-microglobulin （MG）, urine micro-albumin （mALB）, serum soluble intercellular adhesion molecule 1 （slCAM-1） VEGF, von willebrand factor Ⅷ（VWF） and the kidney index in the treatment groups were decreased significantly （P 〈 0.05）, and there was a positive correlation between with 132MG, mALB, SCr and urea nitrogen. Evident alleviation of nephridial tissue injury was appeared in the treatment groups, especially in the middle-dose group and the Iosartan potassium group. Shenshuai Xiezhuo decoction is effective on decreasing the content of SCr, urea nitrogen, β2MG and mALB, and can delay the chronic renal failure. The mechanism may relate with regulating the content of slCAM-1, VEGF and VWF.