本文選題：IgA腎病 + PPAR-γ　； 參考：《復(fù)旦大學(xué)》2014年碩士論文

【摘要】：目的：PPAR-γ作為配體依賴的核因子,除了經(jīng)典的調(diào)節(jié)糖、脂代謝作用外,其抗炎等作用近年受到廣泛關(guān)注。本研究運(yùn)用牛血清γ球蛋白(bovine gammaglobulin, BGG)建立IgA腎病大鼠模型,并觀察PPAR-γ激動(dòng)劑在本病發(fā)生中的作用及其與替米沙坦的協(xié)同治療效果和PPAR-γ與TLR4的相互關(guān)系。方法：77只雄性Lewis大鼠,體重40-55g,飼養(yǎng)溫度25℃,12h晝夜輪替,自由飲食,適應(yīng)性喂養(yǎng)1周后隨機(jī)分為5組：①對(duì)照組(Control, n=18):自由飲用6mmol/l的鹽酸酸化水；②IgA腎病組(IgAN,n=28):自由飲用含0.1%BGG的6mmol/l鹽酸酸化水,連續(xù)9周,其后連續(xù)3天尾靜脈注射1mg BGG;③吡格列酮組(Pio,n=9)：將吡格列酮藥片研磨成粉,每天取1g溶于90m1生理鹽水制成懸濁液,用前搖勻,按3m1/只灌胃4周；④吡格列酮+替米沙坦組(Pio+ARB, n=10):將吡格列酮、替米沙坦藥片研磨成粉,每天分別取1g和0.3g溶于120m1生理鹽水制成懸濁液,用前搖勻,按3m1/只灌胃4周；⑤TLR4抑制劑組(TAK242,n=12)：將配置好的TLR4抑制劑TAK242脂肪乳劑按7.5ml/kg連續(xù)8天尾靜脈注射。分別于第4周末、第6周末、第9周末測(cè)各組大鼠尿白蛋白/肌酐(ACR),顯微鏡下行尿紅細(xì)胞計(jì)數(shù),腹主動(dòng)脈采血檢測(cè)血肌酐和尿素氮,光鏡下觀察腎臟病理?yè)p害,用RT-PCR法檢測(cè)各組腎組織PPAR-γ mRNA和TLR4 mRNA的表達(dá),Western Blot方法檢測(cè)腎組織PPAR-γ蛋白、TLR4蛋白和IL-1p蛋白的表達(dá)情況,免疫熒光檢測(cè)腎小球IgA沉積情況。結(jié)果：①第9周末造模結(jié)束后,模型組尿白蛋白/肌酐明顯高于對(duì)照組(4.45 ±1.33mg/mmol vs 2.89±0.96mg/mmol, P=0.05)。尿紅細(xì)胞計(jì)數(shù)兩組無(wú)明顯差別。與對(duì)照組相比,模型組大鼠SCr、BUN、ALT、AST均無(wú)明顯變化(均P0.05)模型組大鼠與對(duì)照組相比,腎臟組織系膜細(xì)胞及系膜基質(zhì)增生明顯,腎小球橫截面細(xì)胞數(shù)明顯增多(51±4個(gè) vs 41±2個(gè),P0.01),腎小球體積明顯增大,少數(shù)腎小管上皮細(xì)胞腫脹,間質(zhì)輕度炎性細(xì)胞浸潤(rùn)。對(duì)照組腎小球免疫熒光未見IgA沉積,模型組腎小球可見亮綠色團(tuán)塊狀或絮狀I(lǐng)gA沉積。②與對(duì)照組相比,IgA腎病組ACR明顯升高(1.72±0.41mg/mmol vs 1.27±0.15mg/mmol),差異有統(tǒng)計(jì)學(xué)意義(P=0.013)；吡格列酮組尿ACR與對(duì)照組相比無(wú)明顯差異(1.13±0.44mg/mmol vs 1.27±0.15mg/mmol,P=0.41)但顯著低于IgA腎病組(1.13± 0.44mg/mmol vs 1.72±0.41mg/mmol,P=0.015)；吡格列酮+替米沙坦組ACR與對(duì)照組相比無(wú)明顯差異(1.01±0.45mg/mmol vs 1.27±0.15mg/mmol,P=0.41)但顯著低于IgA腎病組(1.01±0.45mg/mmol vs 1.72±0.41mg/mmol,P=0.00)。吡格列酮組與吡格列酮+替米沙坦組ACR無(wú)顯著差異(1.01mg/mmol±0.45 vs 1.13 ±0.44mg/mmol,P=0.18)。與對(duì)照組相比,IgA腎病組腎小球橫截面細(xì)胞數(shù)量明顯增多(50±8個(gè) vs 40±6個(gè),P=0.03),腎小球體積明顯增大,少數(shù)腎小管上皮細(xì)胞腫脹,間質(zhì)輕度炎性細(xì)胞浸潤(rùn)；吡格列酮組與對(duì)照組相比腎小球橫截面細(xì)胞數(shù)量無(wú)明顯差異(46±6個(gè)vs40±6個(gè),P0.05),吡格列酮組與IgA腎病組相比,腎小球橫截面細(xì)胞數(shù)量減少未達(dá)到統(tǒng)計(jì)學(xué)意義(46±6個(gè)vs 50±8個(gè),P=0.23),腎小管基本正常,間質(zhì)未見明顯炎性細(xì)胞浸潤(rùn)；吡格列酮+替米沙坦組與對(duì)照組相比腎小球橫截面細(xì)胞數(shù)量無(wú)明顯差異(41±4個(gè) vs 40±6個(gè),P0.05)但顯著低于IgA腎病組(41±4個(gè) vs 50±8個(gè),P=0.03)。與吡格列酮組相比,減少未達(dá)到統(tǒng)計(jì)學(xué)差異(41±4個(gè) vs 46±6個(gè),P=0.08),腎小管正常,間質(zhì)未見明顯炎性細(xì)胞浸潤(rùn)。與對(duì)照組相比,IgA腎病組血清IL-1β水平和腎組織IL-1β蛋白的表達(dá)均明顯升高(47.45±12.91pg/ml vs 34.49±12.09pg/ml,P=0.01;0.46 ±0.21 vs 0.27±0.10,P=0.04);吡格列酮組與對(duì)照組相比血清IL-1β水平和腎組織IL-1β蛋白的表達(dá)均無(wú)明顯差異(39.06±17.92pg/ml vs 34.49±12.09pg/ml,P0.05；0.32±0.15 vs 0.27±0.10,P=0.45),與IgA腎病組相比,血清IL-1β水平和腎組織IL-1β蛋白的表達(dá)降低均無(wú)統(tǒng)計(jì)學(xué)差異(39.06±17.92pg/ml vs 47.45 ±12.91pg/ml,P=0.30；0.32±0.15 vs 0.46±0.21,P=0.19);吡格列酮+替米沙坦組與對(duì)照組相比,血清IL-1β的水平和腎組織IL-1β蛋白的表達(dá)基本相同(34.49 ±14.55pg/ml vs 34.49±12.09pg/ml,P0.05；0.28±0.09 vs 0.27±0.10,P=0.94)但均顯著低于IgA腎病組(34.49±14.55pg/ml vs 47.45±12.91pg/ml,P=0.04;0.28 ±0.09 vs 0.46±0.21,P=0.04)。與吡格列酮組相比,吡格列酮+替米沙坦組血清IL-1β和腎組織IL-1β蛋白的表達(dá)水平均未達(dá)到統(tǒng)計(jì)學(xué)差異(34.49±14.55pg/ml vs 39.06±17.92pg/ml,P=0.59;0.28±0.09 vs 0.32±0.15,P=0.46)。與對(duì)照組相比,IgA腎病組大鼠腎組織PPAR-γ蛋白的表達(dá)明顯升高(0.64±0.14vs0.42±0.04,P=0.03), PPAR-γmRNA的表達(dá)無(wú)顯著差異(1.20±0.42 vs 0.98±0.03,P=0.39)；吡格列酮組與對(duì)照組相比,PPAR-y蛋白和mRNA的表達(dá)均明顯增加(0.71±0.19vs 0.42±0.04,P=-0.03；1.58±0.20 vs 0.98±0.03,P=-0.001)。與IgA腎病組相比,吡格列酮組PPAR-y蛋白和mRNA的表達(dá)升高未達(dá)到統(tǒng)計(jì)學(xué)意義(0.71±0.19 vs0.64±0.14,P=0.44；1.58±0.20 vs 1.20±0.42,P=0.15)；吡格列酮+替米沙坦組與對(duì)照組、IgA腎病組相比,PPAR-y蛋白和mRNA的表達(dá)均無(wú)統(tǒng)計(jì)學(xué)差異(均P0.05)。與吡格列酮組相比,吡格列酮組+替米沙坦組PPAR-y蛋白和mRNA的表達(dá)均明顯降低(0.56±0.08 vs 0.71±0.19,P=-0.047；1.02±0.17 vs 1.58±0.20,P=0.005)。③與IgA腎病組相比,TLR4抑制劑組ACR顯著降低(1.13± 0.44mg/mmol vs 1.72±0.41mg/mmol, P=0.015),光鏡下系膜細(xì)胞和系膜基質(zhì)明顯減少,腎小球橫截面細(xì)胞數(shù)明顯降低(35±3個(gè) vs 45±3個(gè),P0.01),血清IL-1p和腎組織IL-1p蛋白的表達(dá)無(wú)統(tǒng)計(jì)學(xué)意義(30.20±4.93pg/ml vs 32.99±5.64pg/ml,0.56±0.22 vs 0.63±0.17,均P0.05),PPAR-γ的蛋白表達(dá)明顯增加(0.86±0.20 vs 0.65±0.13,P=0.03),PPAR-γ的mRNA表達(dá)無(wú)統(tǒng)計(jì)學(xué)差異(1.00±0.54vs0.87±0.35,P=0.63)。與IgA腎病組相比,吡格列酮組TLR4蛋白的表達(dá)明顯降低(0.12±0.03 vs 0.21±0.05,P=0.001),TLR4 mRNA的表達(dá)降低未達(dá)到統(tǒng)計(jì)學(xué)差異(0.78±0.21vs0.95±0.09,P=0.13)。結(jié)論：①用口服BGG酸化水9周,尾靜脈注射BGG 3天的方法可以建立輕-中度IgA腎病大鼠模型。②在IgA腎病動(dòng)物模型中,PPAR-γ激動(dòng)劑吡格列酮、血管緊張素受體阻斷劑替米沙坦均可以降低炎癥因子的水平,降低蛋白尿,抑制系膜細(xì)胞和系膜基質(zhì)的增殖,改善IgA腎病。替米沙坦對(duì)吡格列酮的協(xié)同治療效果不明顯。③TLR4抑制劑TAL242可以改善IgA腎病,降低蛋白尿,改善系膜細(xì)胞和系膜基質(zhì)的增殖,在IgA腎病動(dòng)物體內(nèi),TLR4與PPAR-γ可以相互抑制,相互影響。
[Abstract]:Objective: PPAR- gamma, as a ligand dependent nuclear factor, has been widely concerned in recent years, in addition to the classical regulation of sugar and lipid metabolism, and its anti-inflammatory effects have been widely concerned in recent years. This study used bovine serum gamma globulin (bovine gammaglobulin, BGG) to establish a rat model of IgA nephropathy, and observed the role of PPAR- gamma agonist in the pathogenesis of this disease and its effect on telmisartan. Co therapy effect and the relationship between PPAR- gamma and TLR4. Methods: 77 male Lewis rats, weight 40-55g, feeding temperature 25 degrees, 12h circadian rotation, free diet, and free diet after 1 weeks of adaptive feeding, randomly divided into 5 groups: (Control, n=18): free drinking of 6mmol/l in hydrochloric acid water; and IgA nephrotic group (IgAN, n=28): free drinking 0. 1%BGG 6mmol/l hydrochloric acid water for 9 weeks, followed by 3 days of continuous injection of 1mg BGG in the tail vein; 3. Pioglitazone group (Pio, n=9): grind pioglitazone tablets into powder, take 1g dissolved in 90m1 physiological saline daily to make the suspension, shake well before using 3m1/ only for 4 weeks; 4. Pioglitazone + telmisartan group (Pio+ARB, n=10): pioglitazone, tiimi Sartan tablets were grinded into powder, and 1g and 0.3g dissolved in 120m1 saline solution were made every day respectively. Shake well before use and only gavage the stomach for 4 weeks by 3m1/; 5. TLR4 inhibitor group (TAK242, n=12): a configured TLR4 inhibitor, TAK242 fat emulsion, was injected into the tail vein for 8 days by 7.5ml/kg. The rats were measured at the fourth weekend, sixth weekend, and ninth weekend. Urinary albumin / creatinine (ACR), urinary red blood cell count under microscope, blood creatinine and urea nitrogen in abdominal aorta, the pathological damage of kidney was observed under light microscope. The expression of PPAR- gamma mRNA and TLR4 mRNA in renal tissue were detected by RT-PCR. The expression of PPAR- gamma protein, TLR4 protein and IL-1p protein in renal tissue was detected by Western Blot method, and the expression of TLR4 protein and IL-1p protein was detected and immunized. Results: after the end of the ninth weekend model, the urinary albumin / creatinine was significantly higher in the model group than in the control group (4.45 + 1.33mg/mmol vs 2.89 + 0.96mg/mmol, P=0.05). There was no significant difference between the two groups of urine red blood cell count. Compared with the control group, there was no significant change in SCr, BUN, ALT, and AST in the model group (all P0.05) model. Compared with the control group, the proliferation of mesangial cells and mesangial matrix in renal tissue was obvious, and the number of mesangial cross section cells increased significantly (51 + 4 vs 41 + 2, P0.01), the volume of glomeruli was obviously enlarged, a small number of renal tubular epithelial cells were swollen, and the interstitium was mild inflammatory cell infiltration. The glomerular immunofluorescence of the control group was not IgA deposit, and the model group kidney was not found. Compared with the control group, the ACR in the IgA nephropathy group increased significantly (1.72 + 0.41mg/mmol vs 1.27 + 0.15mg/mmol), and the difference was statistically significant (P=0.013). The urine ACR of the pioglitazone group was not significantly different from the control group (1.13 + 0.44mg/mmol vs 1.27 + 0.15mg/mmol, P=0.41) was significantly lower than that of the control group. The disease group (1.13 + 0.44mg/mmol vs 1.72 + 0.41mg/mmol, P=0.015) and pioglitazone + telmisartan group ACR had no significant difference compared with the control group (1.01 + 0.45mg/mmol vs 1.27 + 0.15mg/mmol, P=0.41), but significantly lower than the IgA nephropathy group (1.01 + 0.45mg/mmol vs 1.72 + 0, 0). There was a difference (1.01mg/mmol + 0.45 vs 1.13 + 0.44mg/mmol, P=0.18). Compared with the control group, the number of glomerular cross section cells in the IgA nephropathy group increased significantly (50 + 8 vs 40 + 6, P=0.03), the glomerular volume increased obviously, a few renal tubular epithelial cells were swollen and the interstitium was mild inflammatory cell infiltration, and the pioglitazone group was compared with the control group There was no significant difference in the number of cross section cells (46 + 6 vs40 + 6, P0.05). Compared with the IgA nephropathy group, the number of mesangial cross section cells decreased not statistically (46 + 6 vs 50 + 8, P=0.23). The renal tubules were basically normal and the interstitium was not obviously inflammatory cell infiltration; pioglitazone + telmisartan group was compared with the control group. There was no significant difference in the number of cells in the cross section (41 + 4 vs 40 + 6, P0.05), but significantly lower than the IgA nephropathy group (41 + 4 vs 50 + 8, P=0.03). Compared with the pioglitazone group, the decrease was not statistically significant (41 + 4 vs 46 + 6, P=0.08), renal tubules were normal, and no obvious inflammatory cell infiltration was found in the interstitium. Compared with the control group, the blood of IgA nephropathy group was compared with the control group. The level of IL-1 beta and the expression of IL-1 beta protein in the renal tissue were significantly increased (47.45 + 12.91pg/ml vs 34.49 + 12.09pg/ml, P=0.01; 0.46 + 0.21 vs 0.27 + 0.10, P=0.04), and there was no significant difference between the serum IL-1 beta level and the expression of IL-1 beta protein in the renal tissue compared with the control group (39.06 + 39.06 + 0.10). 0.32 0.15 vs 0.27 + 0.10, P=0.45), compared with the IgA nephropathy group, there was no significant difference in the level of serum IL-1 beta and the expression of IL-1 beta protein in renal tissue (39.06 + 17.92pg/ml vs 47.45 + 12.91pg/ml, P=0.30; 0.32 + 0.15 vs 0.46 + 0.21, P=0.19); and the level of the beta and renal tissue of the pioglitazone + telmisartan group The expression of protein was basically the same (34.49 + 14.55pg/ml vs 34.49 + 12.09pg/ml, P0.05; 0.28 + 0.09 vs 0.27 + 0.10, P=0.94), but significantly lower than that of IgA nephropathy group (34.49 + 14.55pg/ml vs 47.45 + 12.91pg/ml, P=0.04; 0.28 + 0.09 vs 0.46 + 0.21). The expression level of 1 beta protein did not reach statistical difference (34.49 + 14.55pg/ml vs 39.06 + 17.92pg/ml, P=0.59; 0.28 + 0.09 vs 0.32 + 0.15, P=0.46). Compared with the control group, the expression of PPAR- gamma protein in renal tissue of IgA nephropathy rats increased significantly (0.64 + 0.14vs0.42 + 0.04, P= 0.03), PPAR- gamma mRNA was no significant difference (1.20 + 0.42 0.98 0.98) The expression of PPAR-y protein and mRNA increased significantly (0.71 + 0.19vs 0.42 + 0.04, P=-0.03, 1.58 + 0.20 vs 0.98 + 0.03, P=-0.001) in the pioglitazone group (1.58 + 0.20 vs 0.98 +, P=-0.001). The increase of the expression of PPAR-y protein and mRNA in the pioglitazone group was not statistically significant (0.71 + 0.19 vs0.64 + 0.14, P=0.44; 1.58). 0.20 vs 1.20 + 0.42, P=0.15), the expression of PPAR-y protein and mRNA was not significantly different between the pioglitazone + telmisartan group and the control group (P0.05). Compared with the pioglitazone group, the expression of PPAR-y protein and mRNA in the pioglitazone group was significantly decreased (0.56 + 0.08 vs 0.71 + 0.19, P=-0.047; 1.02 + 0.17 vs. 1.58 + 0.20, P=0.005). Compared with IgA nephropathy group, ACR in TLR4 inhibitor group was significantly decreased (1.13 + 0.44mg/mmol vs 1.72 + 0.41mg/mmol, P=0.015), mesangial cells and mesangial matrix decreased significantly under light microscope, and the number of glomerular cross section cells decreased significantly (35 + 3 vs 45 + 3, P0.01). The expression of serum IL-1p and renal tissue IL-1p protein was not statistically significant Significance (30.20 + 4.93pg/ml vs 32.99 + 5.64pg/ml, 0.56 + 0.22 vs 0.63 + 0.17, P0.05), the protein expression of PPAR- gamma increased significantly (0.86 + 0.20 vs 0.65 + 0.13, P=0.03), and PPAR- gamma mRNA expression was not statistically significant (1 + 0.54vs0.87 + 0.35, P=0.63). 0.21 + 0.05, P=0.001), the expression of TLR4 mRNA decreased not statistically (0.78 + 0.21vs0.95 + 0.09, P=0.13). Conclusion: (1) oral BGG acidified water for 9 weeks and 3 days of BGG in the tail vein can establish a rat model of mild to moderate IgA nephropathy. (2) in the animal model of IgA nephropathy, PPAR- gamma agonist, pioglitazone, angiotensin receptor blocker Telmisartan can reduce the level of inflammatory factors, reduce proteinuria, inhibit the proliferation of mesangial cells and mesangial matrix, and improve IgA nephropathy. Telmisartan's synergistic effect on pioglitazone is not obvious. (3) TLR4 inhibitor TAL242 can improve IgA nephropathy, reduce proteinuria, improve the proliferation of mesangial cells and mesangial matrix, in IgA In nephrotic animals, TLR4 and PPAR- gamma can inhibit each other and interact with each other.

【學(xué)位授予單位】：復(fù)旦大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R692

【相似文獻(xiàn)】

相關(guān)期刊論文 前10條

1 任黔川;彭芝蘭;譚欣;;PPARγ在卵巢漿液性囊腺癌中的表達(dá)[J];重慶醫(yī)學(xué);2009年23期

2 張乾勇;PPAR的結(jié)構(gòu)與功能及其生物學(xué)作用[J];國(guó)外醫(yī)學(xué)(衛(wèi)生學(xué)分冊(cè));2000年05期

3 白玉杰,牛丹,趙錦榮,張文紅,呂貫廷,閻小君;Rapid detection of PPAR_γ gene Pro12Ala polymorphism with fluorescence polarization in Chinese population[J];Journal of Medical Colleges of PLA;2003年03期

4 袁平戈;PPARα的主要功能是什么[J];中華肝臟病雜志;2003年05期

5 潘光棟;PPAR-γ及其配體在人體細(xì)胞的分子研究[J];職業(yè)衛(wèi)生與病傷;2003年02期

6 曹廷兵,葉治家,彭家和,鞏燕,黃剛;人PPARγ2 cDNA的克隆及其在大腸桿菌中的表達(dá)純化[J];第三軍醫(yī)大學(xué)學(xué)報(bào);2004年01期

7 王剛,陳繼俊,倪沛洲;PPARα受體亞型與新藥研究[J];藥學(xué)進(jìn)展;2004年01期

8 葉平;過(guò)氧化體增殖物激活型受體(PPAR)與心血管疾病[J];中華心血管病雜志;2004年07期

9 孫曙光,周智廣;PPARγ與1型糖尿病[J];國(guó)外醫(yī)學(xué).內(nèi)分泌學(xué)分冊(cè);2005年02期

10 胡桂芳,武革;PPARγ與2型糖尿病大血管病變的研究進(jìn)展[J];廣東醫(yī)學(xué)院學(xué)報(bào);2005年01期

相關(guān)會(huì)議論文 前10條

1 ;Genetic polymorphisms of PPAR-γ,HHEX,PTPRD,KCNQ1,and SRR affect therapeutic efficacy of Pioglitazone in Chinese Patients with type 2 diabetes[A];傳承與發(fā)展，創(chuàng)湖南省生理科學(xué)事業(yè)的新高——湖南省生理科學(xué)會(huì)2011年度學(xué)術(shù)年會(huì)論文摘要匯編[C];2011年

2 ;Dynamic analysis and ligand binding affinity investigation of PPAR mutations[A];華東六省一市生物化學(xué)與分子生物學(xué)會(huì)2003年學(xué)術(shù)交流會(huì)論文摘要集[C];2003年

3 童南偉;;過(guò)氧化物酶增殖物激活受體(PPAR)a與脂質(zhì)代謝[A];全國(guó)首屆代謝綜合征的基礎(chǔ)與臨床專題學(xué)術(shù)會(huì)議論文匯編[C];2004年

4 王偉銘;章慧娣;劉峰;陳佳韻;陳楠;;PPARγ活化對(duì)腎間質(zhì)成纖維細(xì)胞的作用研究[A];2007年浙滬兩地腎臟病學(xué)術(shù)年會(huì)資料匯編[C];2007年

5 陳剛;林新富;梁繼興;林麗香;沈曉麗;;過(guò)氧化物酶體增殖物激活受體γ(PPARγ)基因多態(tài)性與老年男性骨質(zhì)疏松癥相關(guān)性研究[A];2008內(nèi)分泌代謝性疾病系列研討會(huì)暨中青年英文論壇論文匯編[C];2008年

6 陳剛;林新富;梁繼興;林麗香;沈曉麗;;過(guò)氧化物酶體增殖物激活受體γ(PPARγ)基因多態(tài)性與老年男性骨質(zhì)疏松癥相關(guān)性研究[A];2008中國(guó)醫(yī)師協(xié)會(huì)內(nèi)分泌代謝科醫(yī)師分會(huì)年會(huì)論文匯編[C];2008年

7 李潔;戴愛國(guó);胡瑞成;朱黎明;王梅芳;;PPARγ影響γ-谷氨酰半胱氨酸合成酶活性及表達(dá)在大鼠慢性阻塞性肺疾病中的作用[A];中國(guó)生理學(xué)會(huì)第23屆全國(guó)會(huì)員代表大會(huì)暨生理學(xué)學(xué)術(shù)大會(huì)論文摘要文集[C];2010年

8 管又飛;;脂質(zhì)過(guò)氧化物體增殖物激活受體γ(PPAR γ)與糖尿病腎病[A];中華醫(yī)學(xué)會(huì)腎臟學(xué)分會(huì)2004年年會(huì)暨第二屆全國(guó)中青年腎臟病學(xué)術(shù)會(huì)議專題講座匯編[C];2004年

9 孫莉;尚進(jìn)林;梁浩;程焱;;PPAR全激動(dòng)劑對(duì)小鼠局灶性腦缺血再灌注損傷的保護(hù)作用[A];第十一屆全國(guó)神經(jīng)病學(xué)學(xué)術(shù)會(huì)議論文匯編[C];2008年

10 ;Endothelial PPARγmediates anti-inflammatory actions of rosiglitazone through dissociation of NF-κB[A];中國(guó)生理學(xué)會(huì)心血管生理學(xué)術(shù)研討會(huì)論文集[C];2011年

相關(guān)重要報(bào)紙文章 前3條

1 徐錚奎;發(fā)現(xiàn)PPAR拮抗劑[N];醫(yī)藥經(jīng)濟(jì)報(bào);2012年

2 曾凡新邋林敏;PPAR激動(dòng)劑類抗糖尿病藥研發(fā)喜憂參半[N];中國(guó)醫(yī)藥報(bào);2007年

3 袁松范;開發(fā)PPAR多通道激動(dòng)劑須謹(jǐn)慎[N];中國(guó)醫(yī)藥報(bào);2006年

相關(guān)博士學(xué)位論文 前10條

1 劉炳婷;SUMO特異性蛋白酶1調(diào)控脂肪形成的作用及分子機(jī)制[D];上海交通大學(xué);2014年

2 陳宏;巨噬細(xì)胞PPARγ對(duì)皮膚傷口愈合的作用研究[D];第三軍醫(yī)大學(xué);2015年

3 王伶;高靜水壓刺激對(duì)血小板活化的影響及PPARγ的保護(hù)作用的研究[D];南昌大學(xué);2008年

4 孫晶;PPARγ1對(duì)系膜細(xì)胞外基質(zhì)生成的抑制作用及其機(jī)制[D];復(fù)旦大學(xué);2004年

5 邱龍新;醛糖還原酶通過(guò)調(diào)控肝代謝性核受體PPARα的磷酸化及活性影響脂質(zhì)穩(wěn)態(tài)[D];廈門大學(xué);2009年

6 楊策;PPARγ基因沉默對(duì)細(xì)胞炎癥反應(yīng)的調(diào)控作用[D];第三軍醫(yī)大學(xué);2005年

7 周波;PPAR β/δ對(duì)熱預(yù)處理血管內(nèi)皮細(xì)胞抗氧化損傷的保護(hù)作用及機(jī)制研究[D];中南大學(xué);2012年

8 丁乃崢;PPARδ在大鼠和小鼠早期妊娠子宮中的表達(dá)與調(diào)節(jié)[D];東北農(nóng)業(yè)大學(xué);2002年

9 楊曉波;PPARβ與MMP-9參與蛛網(wǎng)膜下腔出血后早期腦損傷的機(jī)制研究[D];重慶醫(yī)科大學(xué);2014年

10 周吉銀;小檗堿降糖調(diào)脂作用與PPARs/P-TEFb信號(hào)轉(zhuǎn)導(dǎo)通路的關(guān)系[D];第三軍醫(yī)大學(xué);2008年

相關(guān)碩士學(xué)位論文 前10條

1 曹智麗;過(guò)氧化物酶增殖物激活受體α（PPARα）在大鼠酒精性肝病發(fā)生過(guò)程中的變化[D];河北醫(yī)科大學(xué);2015年

2 宋石;miR-27a通過(guò)靶向調(diào)控PPARγ對(duì)酒精誘導(dǎo)大鼠BMSC分化的影響[D];鄭州大學(xué);2015年

3 鄒佳楠;PPAR-γ在IgA腎病發(fā)生中的作用及其機(jī)理研究[D];復(fù)旦大學(xué);2014年

4 陶曉燕;PPAR δ激動(dòng)劑和siRNA對(duì)大鼠骨髓基質(zhì)干細(xì)胞及成骨細(xì)胞分化和礦化的作用研究[D];安徽醫(yī)科大學(xué);2015年

5 于飛;新型PPARγ激動(dòng)劑對(duì)人腎癌細(xì)胞增殖抑制及其機(jī)制的研究[D];中國(guó)人民解放軍軍事醫(yī)學(xué)科學(xué)院;2015年

6 何修界;PPARγ激活對(duì)GDM小鼠胎盤脂肪酸運(yùn)輸?shù)鞍妆磉_(dá)水平的影響[D];安徽醫(yī)科大學(xué);2015年

7 魏璇;PPARγ通過(guò)對(duì)RUVBL2表達(dá)調(diào)控影響脂聯(lián)素分泌的研究[D];華中農(nóng)業(yè)大學(xué);2015年

8 游潔冰;PPARγ激動(dòng)劑、胰島素通過(guò)上調(diào)負(fù)性炎性因子TIPE2的表達(dá)抑制高糖、Aβ1-40引起的炎性反應(yīng)及神經(jīng)細(xì)胞調(diào)亡[D];山東大學(xué);2015年

9 劉常為;CTGF、COL-I、PPARγ在卵巢細(xì)胞外基質(zhì)的表達(dá)及與多囊卵巢綜合征的關(guān)系[D];暨南大學(xué);2015年

10 曹小潔;TLR4通過(guò)PPARγ下調(diào)ABCG1表達(dá)促進(jìn)血管平滑肌細(xì)胞內(nèi)炎癥反應(yīng)及脂質(zhì)沉積[D];第三軍醫(yī)大學(xué);2015年

，

本文編號(hào)：1866418