摘要
目的采用5/6肾切除法建立大鼠慢性肾衰动物模型,以中药复方剂"降浊颗粒"治疗,观察并评价其对CRF肠道免疫功能的影响。方法 Wistar大鼠造模后分为降浊颗粒高、中、低剂量组,贝那普利组,假手术组,模型对照组,分别给予降浊颗粒4.05、8.10、16.20g·kg^(-1)·d^(-1)及贝那普利1.2mg·kg^(-1)·d^(-1)灌胃,假手术组及模型对照组予生理盐水2mL·kg^(-1)·d^(-1)灌胃,疗程60d。观察治疗前后肌酐、尿素氮变化,同时测定血清及肠道SIgA水平,以及mRNA及蛋白表达。结果贝那普利组、降浊颗粒各剂量组血清BUN、Scr水平明显低于模型对照组(P<0.05);ELISA、蛋白表达与RT-PCR结果比较,贝那普利组、降浊颗粒各剂量组与模型对照组比较,肠道IgA蛋白和mRNA表达显著升高(P<0.05),降浊颗粒高、中剂量组与贝那普利组比较,明显升高(P<0.05)。结论降浊颗粒有独立于具有改善肾功能的作用,此外对CRF肠道免疫功能也有一定的改善作用。
Objective To establish a rat model of chronic renal failure (CRF) by using 5/6 subtotal nephrectomy method, then observe and evaluate the effect of Turbidity-reducing Granule on the intestinal immune function of rats with CRF. Methods CRF model Wistar rats were divided into high,medium and low dose group, sham operation group, and model control group, respec- tively given Turbidity-reducing Granule 4.05,8.10,16.20 g· kg-1 · d-1. Benazepril group was given 2 mL/d (1.2 mg/d) Benaze- pril suspension fed;model control group and the sham group are saline 2 mL/d orally. The rats were observed before and after treat- ment of signs and general condition, serum BUN, Scr changes, and pathological changes were observed under microscope. ELISA method were used to detect serum and intestinal SIgA. Results Turbidity-reducing Granule reduced the level of serum BUN,Scr in rats with CRF, there were statistically significant differences of Benazepril group and high, medium,low dose of Turbidity-reducing Granule group compared with model group(P〈0.05). Compared with the model group, the intestinal SIgA of Benazepril group and low, middle,high dose of group increased significantly(P〈0.05) ;intestinal SIgA in, middle and high dose group were significantly increased compared with Benazepril group(P〈0.05). Conclusion Turbidity-reducing Granule could improve renal function and in- testinal immune function.
出处
《重庆医学》
CAS
北大核心
2016年第3期329-331,335,共4页
Chongqing medicine
基金
2013年云南省自然科学基金(2011FZ258)
关键词
肾功能衰竭
慢性
中药疗法
降浊颗粒
肠道免疫功能
kidney failure, chronic
drug therapy(TCD)
Turbidity-reducing Granule
intestinal IgA