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作 者:邹美南[1] 郑平[1] 李中桂[1] 郑琳[1] 魏俊婷[1] 王曼茹[1] 江霞[1] 易铁钢[2] 李顺民[2] 陈剑平[1] 张尚斌[1]
机构地区:[1]深圳市中医院中药实验室深圳市医院中药制剂研究重点实验室,深圳518033 [2]深圳市中医院肾病科,深圳518033
出 处:《河北中医药学报》2017年第4期7-11,共5页Journal of Hebei Traditional Chinese Medicine and Pharmacology
基 金:广东省自然科学基金项目:No.2015A030310247;广东省中医药局项目:No.20162124;深圳市科技计划项目:No.JSGG20141017103353178;ZDSYS201606081515458;JCYJ20160428182041577
摘 要:目的:研究健脾益肾丸对5/6肾切除大鼠模型肾损伤的改善作用,并分析探讨其可能存在的机制。方法:40只SD大鼠随机分为假手术组、模型对照组、健脾益肾丸低剂量组(2.06 g/kg·d^(-1))、健脾益肾丸高剂量组(10.89 g/kg·d^(-1))、培哚普利组(4 mg/kg·d^(-1)),每组10只。造模4个月后开始给药,连续给药6周。6周后处死大鼠,留取血清,采用酶联免疫吸附试验法检测血肌酐(Scr)、尿素氮(BUN);采用实时荧光定量PCR法检测肾组织TGF-β1、Smad2、Smad3 mRNA基因表达。结果:健脾益肾丸不同剂量均可明显降低大鼠血清Scr、BUN水平(P<0.01/P<0.05),下调TGF-β1、Smad2、Smad3 mRNA基因表达(P<0.01);培哚普利作为西药阳性对照,可明显降低大鼠血清Scr、BUN水平(P<0.01/P<0.05),下调TGF-β1、Smad2、Smad3 mRNA基因表达(P<0.01)。结论:健脾益肾丸能有效改善5/6肾切除慢性肾衰大鼠模型肾功能;其机制可能与下调TGF-β1、Smad2、Smad3水平,从而抑制过度激活的TGF-β1/Smads信号通路有关。Objective: to study the improvement function of Jianpi Yishen Pill on renal injury of 5/6 nephrectomy in rats, and to explore the possible mechanism.Methods: 40 SD rats were randomly divided into sham operation group, control group, low dose of Jianpi Yishen Pill group (2.06 g/kg·d-1), high dose group (10.89 g/kg·d-1), and Perindopril group (4 mg/kg·d-1), 10 rats a group.4 months after models finished, administration began and it lasted for 6 weeks.The rats were then killed with serum taken.Enzyme-linked immunosorbent test was used to detect serum creatinine (Scr) and blood urea nitrogen (BUN), and real-time fluorescence quantification PCR to detect gene expressions of TGF-β1, Smad2, Smad3 and mRNA.Results: both high and low dose of Jianpi Yishen Pill could significantly decrease Scr and BUN (P〈0.01/P〈0.05) and lower TGF-β1, Smad2, Smad3 and mRNA expressions (P〈0.01);Perindopril could significantly decrease Scr and BUN (P〈0.01/P〈0.05) and lower TGF-β1, Smad2, Smad3 and mRNA expressions (P〈0.01).Conclusion: Jianpi Yishen Pill can effectively improve the renal function of 5/6 nephrectomy in rats with chronic renal failure, whose mechanism may be related to inhibiting the excessive activated TGF-β1/Smads signal path through lowering TGF-β1, Smad2 and Smad3.
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