本文關(guān)鍵詞： 慢性腎功能衰竭 腎衰飲 CTGF FN TNF-α IL-6　出處：《遼寧中醫(yī)藥大學(xué)》2016年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:通過觀察腎衰飲對腺嘌呤致慢性腎功能衰竭大鼠腎臟CTGF、FN、TNF-α及IL-6的表達(dá),探討腎衰飲延緩慢性腎功能衰竭的藥效學(xué)機(jī)制。材料與方法:SPF級SD雄性大鼠60只(體重180±20g),按照Yokozawa法制備大鼠腎衰模型,12只為正常組,其余為造模組。模型制備成功后將所有造膜大鼠再隨機(jī)分為模型組、腎衰飲組、尿毒清組,分別予以中藥復(fù)方腎衰飲、中成藥尿毒清顆粒灌胃,模型組與正常組予Na Cl日一次灌胃,連續(xù)給藥4周,記錄大鼠體重、活動狀態(tài)及外觀變化,給藥結(jié)束后腹主動脈采血驗血肌酐(SCr)、尿素氮(BUN)。取左腎組織,肉眼觀察其形態(tài),光鏡觀察其病理變化。免疫組織化學(xué)法檢測CTGF、FN的表達(dá)水平,ELISA法檢測TNF-α、IL-6的表達(dá)水平,最后對各指標(biāo)進(jìn)行數(shù)據(jù)統(tǒng)計分析。結(jié)果:1.模型組CTGF、FN蛋白表達(dá)增強(qiáng),與正常組比較有極顯著性差異(P0.01);與模型組比較,腎衰飲組CTGF、FN表達(dá)下降(P0.05),尿毒清組CTGF、FN則沒有顯著性差異(P0.05);與尿毒清組比較,腎衰飲組CTGF、FN表達(dá)下降有顯著性差異(P0.05)。2.模型組TNF-α的蛋白表達(dá)增強(qiáng),與正常組比較有顯著性差異(P0.05);與模型組比較,腎衰飲組和尿毒清組TNF-α的蛋白表達(dá)明顯降低(P0.01);與尿毒清組比較,腎衰飲組TNF-α的蛋白表達(dá)降低(P0.01)。與模型組比較,腎衰飲組IL-6的蛋白表達(dá)減弱(P0.01),尿毒清組IL-6的表達(dá)則沒有顯著性差異(P0.05);與尿毒清組比較,腎衰飲組IL-6表達(dá)下降有顯著性差異(P0.01)。3.模型組SCr、BUN水平升高,與正常組比較有極顯著性差異(P0.01);與模型組比較,腎衰飲組和尿毒清組SCr、BUN水平明顯降低(P0.01);與尿毒清組比較,腎衰飲組SCr水平降低(P0.05),但BUN水平無顯著性差異(P0.05)。4.與正常組比較,模型組病理改變最明顯,其次為尿毒清組,腎衰飲組的改變最輕微。結(jié)論:腎衰飲能有效抑制TGF-β1誘導(dǎo)的下游因子CTGF表達(dá),降低FN、TNF-α、IL-6水平,以抑制腎纖維化的發(fā)生、發(fā)展,為腎衰飲有效治療慢性腎功能衰竭提供客觀依據(jù)。
[Abstract]:Objective: to observe the expression of TNF- 偽 and IL-6 in kidney of rats with chronic renal failure induced by adenine by Shenshuai decoction. To explore the pharmacodynamic mechanism of Shenshuiyin in delaying chronic renal failure. Materials and methods 60 SD male rats of SPF grade (body weight 180 鹵20g) were used. According to the Yokozawa method, 12 rats with renal failure were divided into normal group and model group. After the establishment of the model, all the membrane-making rats were randomly divided into three groups: model group, Shenshuai decoction group and Niaoduqing group. The rats in the model group and the normal group were treated with sodium chloride once a day for 4 weeks. The body weight, activity state and appearance of the rats were recorded. At the end of administration, blood samples were collected from abdominal aorta for examination of creatinine, bun, bun. The left renal tissue was taken, the morphology was observed with naked eye, the pathological changes were observed by light microscope, and the CTGF was detected by immunohistochemical method. The expression level of FN and the expression of TNF- 偽 IL-6 were detected by Elisa. Finally, the data of each index were statistically analyzed. Results: 1. The expression of CTGFFN protein was enhanced in model group. Compared with the normal group, there was a significant difference between the two groups (P 0.01). Compared with the model group, the expression of CTGFFN in Shenshuai decoction group was decreased (P 0.05), while that in Niaoduqing group was not significantly different (P 0.05). Compared with Niaoduqing group, the expression of CTGFFN in Shenshuai decoction group was significantly lower than that in Niaoduqing group (P 0.05). 2. The protein expression of TNF- 偽 was increased in model group. Compared with the normal group, there was a significant difference (P 0.05). Compared with the model group, the protein expression of TNF- 偽 in Shenshuiyin group and Niaoduqing group was significantly lower than that in model group. Compared with Niaoduqing group, the protein expression of TNF- 偽 in Shenshuai decoction group was lower than that in model group. Compared with model group, the protein expression of IL-6 in Shenshuai decoction group was decreased (P 0.01). There was no significant difference in the expression of IL-6 in Niaoduqing group (P 0.05). Compared with Niaoduqing group, the expression of IL-6 in Shenshuiyin group was significantly lower than that in Niaoduqing group. The level of IL-6 bun in model group was higher than that in model group. Compared with the normal group, there was a significant difference between the two groups (P 0.01). Compared with the model group, the level of SCR bun in Shenshuiyin group and Niaoduqing group was significantly lower than that in model group. Compared with Niaoduqing group, the SCr level of Shenshuiyin group decreased P0.05N, but there was no significant difference in BUN level. Compared with the normal group, the pathological changes of the model group were the most obvious. Conclusion: Shenshuai decoction can effectively inhibit the expression of downstream factor CTGF induced by TGF- 尾 1 and decrease the level of TNF- 偽 IL-6. To inhibit the occurrence and development of renal fibrosis and provide objective basis for the effective treatment of chronic renal failure with Shenshuai decoction.
【學(xué)位授予單位】：遼寧中醫(yī)藥大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2016
【分類號】：R277.5

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