【摘要】：目的:觀察球型脂聯(lián)素對2型糖尿病大鼠腎臟病變中的TGF-β1、Smad3、Smad7等相關(guān)因子表達(dá)的影響,探討球型脂聯(lián)素對2型糖尿病大鼠腎臟病變發(fā)生、發(fā)展過程中的保護(hù)作用機(jī)制。方法:將雄性SD大鼠按體質(zhì)量隨機(jī)分為正常對照組(NC組)以及模型組。NC組給予普通飼料喂養(yǎng)。模型組給予高糖、高脂飼料喂養(yǎng),8周后,按30mg/kg分別給予濃度為1%的鏈脲佐菌素腹腔注射。NC組予等量檸檬酸-檸檬酸鈉緩沖液。4周后測空腹血糖均高于16.7mmol/L,并出現(xiàn)DM的臨床表現(xiàn),表明T2DM模型已成功建立。繼續(xù)飼養(yǎng)6周后檢測模型組大鼠尿蛋白陽性,取腎臟進(jìn)行病理觀察,2型糖尿病腎病模型成功建立。造模成功后,將模型組隨機(jī)分為糖尿病組(DM組)、脂聯(lián)素組(AD組),AD組給予球型脂聯(lián)素腹腔注射10ug/kg,每日1次,DM組給予同等量生理鹽水腹腔注射每日1次,各組分別于實(shí)驗(yàn)第4周、8周、12周末,留取血標(biāo)本,檢測血糖;留取尿標(biāo)本,檢測尿肌酐、尿蛋白;然后取腎臟組織,稱重并計(jì)算腎重指數(shù)。觀察病理結(jié)果,測定TGF-β1、Smad3、Smad7 m RNA、蛋白表達(dá)水平。結(jié)果:1.與NC組、AD組相比,DM組同期大鼠空腹血糖、24h尿白蛋白、尿肌酐和腎重/體重顯著升高(P0.05);2.TGF-β1、Smad3的表達(dá)在DM組中均明顯高于NC組與AD組(P0.05);3.Smad7的表達(dá)在DM組中均明顯低于NC組與AD組(P0.05);結(jié)論:1.TGF-β1、Smad3在糖尿病腎病中起致病作用,Smad7起保護(hù)作用2.脂聯(lián)素通過下調(diào)TGF-β1、Smad3的表達(dá),上調(diào)Smad7的表達(dá),抑制腎臟纖維化,延緩甚至逆轉(zhuǎn)糖尿病腎病的進(jìn)展。
[Abstract]:Aim: to observe the effect of globular adiponectin on the expression of TGF- 尾 1, Smad3,Smad7 and other related factors in renal lesions of type 2 diabetic rats, and to explore the protective mechanism of globular adiponectin on the occurrence and development of renal pathological changes in type 2 diabetic rats. Methods: male SD rats were randomly divided into normal control group (NC group) and model group according to body weight. NC group was fed with ordinary diet. The model group was fed with high glucose and high fat diet. After 8 weeks, streptozotocin of 1% concentration was injected intraperitoneally according to 30mg/kg. The NC group was given the same amount of citric acid-sodium citrate buffer. 4 weeks later, the fasting blood glucose was higher than 16.7 mmol / L, and the blood glucose of the model group was higher than 16.7 mmol / L after 4 weeks. The clinical manifestations of DM showed that the T2DM model had been successfully established. After 6 weeks of feeding, the urine protein of rats in the model group was detected and the kidney was taken for pathological observation. The model of type 2 diabetic nephropathy was successfully established. After successful establishment of the model, the model group was randomly divided into diabetic group (DM group), adiponectin group (AD group), AD group) received intraperitoneal injection of 10 ug / kg adiponectin once a day, and DM group received the same amount of saline intraperitoneal injection once a day. Blood samples were collected from each group at the 4th week, 8th week and 12th weekend to detect blood glucose. Urine samples were collected, urine creatinine and protein were measured, and kidney tissue was taken to weigh and calculate renal weight index. The expression levels of TGF- 尾 1 and Smad3,Smad7 m RNA, protein were measured. Results: 1. Compared with NC group and AD group, fasting blood glucose, 24-hour urinary albumin, urine creatinine and renal weight / body weight in DM group were significantly higher than those in DM group and AD group (P0.05). 2. The expression of TGF-尾 1 and Smad3 in DM group was significantly higher than that in NC group and AD group (P0.05). The expression of 3.Smad7 in DM group was significantly lower than that in NC group and AD group (P0.05). Conclusion: 1. TGF-尾 1 and Smad3 play a pathogenic role in diabetic nephropathy, and Smad7 play a protective role in diabetic nephropathy. Adiponectin can down-regulate the expression of TGF- 尾 1 and Smad3, up-regulate the expression of Smad7, inhibit renal fibrosis and delay or even reverse the progression of diabetic nephropathy.
【學(xué)位授予單位】：山西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R587.2;R692.9

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本文編號：2449730