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尔肾康对肾病综合征大鼠模型系膜增殖的影响
引用本文:王海生,张亚荣,刁娟娟.尔肾康对肾病综合征大鼠模型系膜增殖的影响[J].山西中医,2009,25(10):47-49.
作者姓名:王海生  张亚荣  刁娟娟
作者单位:1. 福建中医学院,福州,350108
2. 山东省中医院
摘    要:目的:观察中药尔肾康对肾病综合征大鼠模型系膜增殖的影响,探讨其治疗机制。方法:选取Wistar大鼠,采用阿霉素慢性肾病模型,分别用强的松和中药合强的松进行治疗,并设对照组,连续给药12周,测定24h尿蛋白定量、血生化及血、尿TNF—α,观察肾脏病理变化。结果:中药合激素组24h尿蛋白定量呈明显低值,与模型组相比有极显著性差异(P〈0.01),与激素组相比较有明显差异(P〈0.05);中药合激素组明显降低大鼠血、尿TNF—α浓度,与激素组比较也有明显差异(P〈0.05);中药合激素组同激素组比较有显著升高白蛋白作用(P〈0.05);病理切片发现,中药合激素组与模型组、激素组比较,肾小球轮廓清晰,系膜细胞和系膜基质增生不明显,肾小管内未见有蛋白管型。结论:尔肾康有明显抑制系膜增殖的作用,机理可能是促进白蛋白的合成,减少白蛋白在肾小管处的分解,抑制TNF—α的分泌。

关 键 词:尔肾康  肾病综合征  系膜增殖  TNF-α  实验研究

Effect of Er-shen-kang on Intercapillary Hyperplasia in Nephrotic Syndrome Rats
Institution:WANG Hai-sheng, ZHANG Ya-rong, DIAO Juan-juan (Fujian TCM College, Fuzhou, 350108, China)
Abstract:Objective:To observe the curative effect of Er-shen-kang on intercapillary hyperplasia in nephrotic syndrome rats, and investigate its mechanism of action. Method: Wistar rats were made into chronic nephropathy models with Adriamyein. Control group was treated by prednisone, treatment group was done by Chinese medicine and prednisone. The treatment course included 12 weeks. Then 24 h urinary protein quantity, blood biochemistry, and TNF -α in blood and urine were detected, and renal pathological change was observed. Result: 24 h urinary protein quantity decreased markedly in treatment group. Extreme significant difference showed up between treatment group and model group ( P 〈 0.01 ), and significant difference did between treatment group and control group (P 〈0. 05). TNF-α in blood and urine stepped down markedly in treatment group, and significant difference showed up between it and control group (P 〈 0.05). Albumin stepped up markedly in treatment group more than in control group ( P 〈 0. 05 ). Pathological section indicated that edge of acinus renis was sharp, hyperplasy of intercapillary cells and base was not obvious, and protein cast did not emerge in nephric tubule in treatment group, model group and control group. Conclusion: Er-shen-kang can restrain intercapillary hyperplasia markedly. The mechanism may be promoting synthesis of albumin, reducing albuminolysis in nephric tubule, and inhibiting secretion of TNF - α.
Keywords:Er-shen-kang  nephrotic syndrome  intercapillary hyperplasia  TNF-α
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