本文關(guān)鍵詞：PCOS大鼠模型的建立及鹽酸吡咯列酮對PCOS大鼠下丘腦及卵巢中瘦素受體表達的影響　出處：《福建醫(yī)科大學(xué)》2008年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 多囊卵巢綜合征 鹽酸吡咯列酮 胰島素抵抗 瘦素受體 瘦素抵抗

【摘要】： 【目的】評價來曲唑誘導(dǎo)多囊卵巢綜合征(Polysystic Ovary Syndrome,PCOS)大鼠模型的意義,分析瘦素受體(leptin receptor,Lep R)與PCOS的關(guān)系,研究鹽酸吡咯列酮對PCOS大鼠下丘腦和卵巢中Lep R的影響。 【方法】將30只雌性SD大鼠分為三組:正常對照組、PCOS組、鹽酸吡咯列酮干預(yù)組。測定各組大鼠血清T、LH、FG、INS、LEP水平,通過免疫組織化學(xué)、Real Time RT PCR方法檢測各組大鼠下丘腦、卵巢中Lep R的相對表達。 【結(jié)果】1.來曲唑誘導(dǎo)PCOS大鼠模型,符合PCOS的內(nèi)分泌特征,具備高胰島素血癥和高瘦素血癥。2. PCOS大鼠經(jīng)鹽酸吡咯列酮干預(yù)后血清T、LH、INS、LEP明顯下降(P 0.05)。相關(guān)分析得出:T與HOMA-IR、INS均呈正相關(guān)(rs=0.443,0.366;P 0.05)。3.經(jīng)免疫組織化學(xué)、Real Time RT PCR方法相對定量檢測各組下丘腦、卵巢中Lep R的表達,提示PCOS大鼠下丘腦Lep R表達較正常對照組減弱(P 0.05),鹽酸吡咯列酮干預(yù)后下丘腦Lep R表達增強(P 0.05)。而卵巢中Lep R表達與下丘腦正好相反,即PCOS大鼠卵巢中Lep R表達較正常對照組增強(P 0.05),經(jīng)鹽酸吡咯列酮干預(yù)后卵巢Lep R表達減弱(P 0.05)。 【結(jié)論】1.來曲唑誘導(dǎo)PCOS大鼠模型是目前研究PCOS發(fā)病機制,胰島素抵抗、瘦素抵抗的發(fā)生機制較合適的建立方法。2. PCOS大鼠下丘腦Lep R表達減低導(dǎo)致瘦素抵抗,可能是PCOS產(chǎn)生無排卵、月經(jīng)紊亂等內(nèi)分泌紊亂的主要原因。PCOS大鼠卵巢中Lep R表達增強,導(dǎo)致瘦素的生理作用增強,即增強了瘦素對卵巢分泌雌、孕激素功能的抑制作用,可能是PCOS大鼠不排卵,生育力下降的原因。3.胰島素增敏劑—鹽酸吡咯列酮改善PCOS大鼠高胰島素血癥、高瘦素血癥、高雄激素血癥等內(nèi)分泌異常的同時使PCOS大鼠下丘腦Lep R表達增強,有效改善了瘦素抵抗;同時卵巢LepR表達下調(diào),減弱了瘦素對卵巢分泌雌、孕激素功能的抑制作用,改善卵巢性激素分泌的功能。
[Abstract]:[objective] to evaluate the significance of letrozole induced polycystic Ovary Syndromes (PCOS) rat model. To study the effect of pyrrolidone hydrochloride on Lep in hypothalamus and ovary of PCOS rats by analyzing the relationship between leptin receptor leptin receptor Lep R) and PCOS. The influence of R. [methods] Thirty female Sprague-Dawley rats were divided into three groups: normal control group, PCOS group and pyrrolidone hydrochloride intervention group. The relative expression of Lep R in hypothalamus and ovary was detected by real Time RT PCR method. [results] 1. Letrozole induced PCOS rat model, according to the endocrine characteristics of PCOS. 2. The rats with hyperinsulinemia and hyperleptinemia. 2. PCOS rats were treated with pyrrolidone hydrochloride. LEP decreased significantly (P 0.05). Correlation analysis showed that there was a positive correlation between LEP and HOMA-IRINS. The expression of Lep R in hypothalamus and ovary was detected by real Time RT PCR method. The results suggest that the expression of Lep R in hypothalamus of PCOS rats is lower than that of normal control group (P 0.05). The expression of Lep R in hypothalamus increased after the intervention of pyrrolidone hydrochloride, but the expression of Lep R in ovary was opposite to that in hypothalamus. The expression of Lep R in the ovary of PCOS rats was significantly higher than that of the normal control group (P 0.05), and the expression of Lep R in the ovary was decreased after the intervention of pyrrolidone hydrochloride. [conclusion] 1.The rat model of PCOS induced by letrozole is the current study of the pathogenesis of PCOS, insulin resistance. 2. The mechanism of leptin resistance is more suitable to establish method .2.The decrease of Lep R expression in hypothalamus of PCOS rats may lead to leptin resistance, which may be caused by PCOS anovulation. The main reason of endocrine disorder, such as menstrual disorder, is that the expression of Lep R in the ovary of PCOS rats is increased, which leads to the enhancement of the physiological function of leptin, that is, it enhances the secretion of leptin to the ovary. The inhibition of progesterone function may be the reason for the decline of fertility and anovulation in PCOS rats. 3. The insulin sensitizer, pyrrolidone hydrochloride, can improve hyperinsulinemia and hyperleptinemia in PCOS rats. The endocrine abnormalities such as hyperandrogenemia increased the expression of Lep R in hypothalamus of PCOS rats and effectively improved leptin resistance. At the same time, the expression of LepR in the ovary was down-regulated, which weakened the inhibitory effect of leptin on the secretion of estrogen and progesterone, and improved the function of the secretion of ovarian sex hormone.
【學(xué)位授予單位】：福建醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2008
【分類號】：R711.75;R-332

【參考文獻】

相關(guān)期刊論文 前7條

1 施亞雄,鄭善德,徐惠貞,李永加;PPARγ激動劑羅格列酮改善胰島素抵抗治療肥胖型多囊卵巢綜合征的臨床研究[J];第二軍醫(yī)大學(xué)學(xué)報;2003年05期

2 馮光榮,尤昭玲,賀冰,羅嵐;多囊卵巢綜合征動物模型建立的研究現(xiàn)狀與展望[J];湖南中醫(yī)藥導(dǎo)報;2004年01期

3 朱輝,倪江,姚蘭春,邊淑玲,姜杰,黃淇;大鼠多囊卵巢動物模型的實驗研究[J];哈爾濱醫(yī)科大學(xué)學(xué)報;1999年03期

4 唐本雄,曹纘孫,毛文軍;多囊卵巢綜合征婦女內(nèi)源性胰島素釋放與睪酮反應(yīng)的相關(guān)性研究[J];中國病理生理雜志;1993年01期

5 胡顏霞;張展;賈莉婷;;來曲唑誘導(dǎo)多囊卵巢綜合征大鼠模型的研究[J];中國婦幼保健;2006年07期

6 吳效科,周珊英,蘇延華;多囊卵巢綜合征患者的胰島素抵抗[J];中華婦產(chǎn)科雜志;1999年11期

7 張以文;多囊卵巢綜合征的現(xiàn)代概念[J];中華婦產(chǎn)科雜志;2004年09期

，

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