本文選題：糖尿病腎病 + 人腎小球系膜細(xì)胞��； 參考：《桂林醫(yī)學(xué)院》2017年碩士論文

【摘要】：目的:觀察絞股藍(lán)皂苷(gypenosides,GP)對晚期糖基化終末產(chǎn)物(advanced glycation endproducts,AGEs)誘導(dǎo)下人腎小球系膜細(xì)胞(human mesangial cells,HMCs)中晚期糖基化終末產(chǎn)物受體(RAGE)及轉(zhuǎn)化生長因子-β1(TGF-β1)表達(dá)的影響。方法:將體外培養(yǎng)的(含有15%胎牛血清的DMEM低糖培養(yǎng)液)的人腎小球系膜細(xì)胞(HMCs)分成四個實驗組:正常組、模型組、GP組、陽性對照組。除正常組外,根據(jù)前期課題MTT實驗結(jié)果余下三組均再給予200mg·L-1 AGEs刺激。此外,GP組中再分別加入由低至高三個不同濃度的GP(25、75、175 mg·L-1)進行干預(yù),陽性對照組中加入氨基胍鹽酸鹽(0.1mmol·L-1)進行干預(yù)。同步孵育72小時后,應(yīng)用Western blotting技術(shù)檢測各實驗組中RAGE和TGF-β1蛋白的表達(dá)水平;應(yīng)用RT-PCR技術(shù)檢測各實驗組中RAGE和TGF-β1 mRNA的表達(dá)水平。結(jié)果:與正常組比較,體外培養(yǎng)的HMCs,模型組中AGEs誘導(dǎo)下HMCs中RAGE、TGF-β1蛋白及mRNA異常高表達(dá),差異顯著(P均0.01);與模型組比較,GP組中GP可明顯下調(diào)HMCs中RAGE、TGF-β1蛋白及mRNA的表達(dá),并呈濃度依賴性,差異有統(tǒng)計學(xué)意義(P均0.01)。結(jié)論:GP可降低AGEs誘導(dǎo)下HMCs中RAGE的異常高表達(dá),阻斷AGEs-RAGE經(jīng)典的信號通路,并下調(diào)下游轉(zhuǎn)化生長因子-β1的表達(dá)活性,進而延緩DN纖維化這一病理進程,對早期DN防治可發(fā)揮一定積極地意義。
[Abstract]:Aim: to observe the effect of GypenosidesGypenosidesGPon on the expression of advanced glycation endproducts (ages) and transforming growth factor- 尾 1TGF- 尾 1 (TGF- 尾 1) in human Mesangial cells (HMCs) induced by advanced glycosylation end product receptor (RAGEG) and transforming growth factor 尾 1TGF- 尾 1 (TGF- 尾 1) in human Mesangial cells. Methods: human glomerular Mesangial cells cultured in vitro (DMEM low glucose medium containing 15% fetal bovine serum) were divided into four groups: normal group, model group and positive control group. In addition to the normal group, the other three groups were stimulated with 200mg L -1 AGEs according to the results of the previous MTT experiment. In addition, three different concentrations of GPX 2575175 mg / L were added to GP group and 0.1 mmol / L aminoguanidine hydrochloride was added to positive control group. After 72 hours of incubation, the expression of RAGE and TGF- 尾 1 protein in each experimental group was detected by Western blotting technique, and the expression level of RAGE and TGF- 尾 1 mRNA in each experimental group was detected by RT-PCR technique. Results: compared with the normal group, the expression of RAGETGF- 尾 1 protein and mRNA in HMCs induced by AGEs in the model group was significantly higher than that in the normal group (P 0.01), and the expression of RAGEN TGF- 尾 1 protein and mRNA in HMCs was significantly down-regulated in the GP group compared with the model group. The difference was statistically significant (P < 0.01). Conclusion the AGEs induced abnormal high expression of RAGE in HMCs can be inhibited by AGEs, the classical signal pathway of AGEs-RAGE is blocked, and the activity of transforming growth factor-尾 1 is down-regulated, which can delay the pathological process of DN fibrosis. The prevention and treatment of early DN can play a positive role.
【學(xué)位授予單位】：桂林醫(yī)學(xué)院
【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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相關(guān)期刊論文 前10條

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