本文選題：逼尿肌無力 + 骨髓間充質干細胞��； 參考：《第三軍醫(yī)大學》2015年碩士論文

【摘要】：一、目的:探討在凍傷引起的逼尿肌無力(acontractile detrusor,ACD)大鼠模型中,丁酸鈉(Sodium Butyrate)聯(lián)合大鼠骨髓間充質干細胞(rat bone marrow-derived mesenchymal stem cells,BM-MSCs)通過膀胱壁注射法改善逼尿肌無力的可能性。二、材料與方法:85只(Sprague-Dawley,SD)雌性大鼠,分為5組,每組17只。用68只大鼠建立低溫誘導的膀胱逼尿肌無力(acontractile detrusor,ACD)模型。模型建立完成后,分別立即將0.2ml磷酸鹽緩沖鹽水(phosphate-buffered saline,PBS),0.2ml含有3×106 M丁酸鈉(Sodium Butyrate)的PBS,0.2ml含有1×106大鼠骨髓間充質干細胞(BM-MSCs)的PBS,0.2ml含有3×106 M丁酸鈉及1×106大鼠骨髓間充質干細胞的PBS注入各組大鼠膀胱壁內,剩余17只未處理大鼠作為正常對照組。14天后檢測各組大鼠膀胱排尿功能,逼尿肌肌條收縮力,各組大鼠膀胱壁組織學改變情況用HE染色檢測,RT-PCR及Western blot檢測平滑肌收縮相關蛋白(α-SMA、Calponin和SM-MHC)的表達情況。三、結果:低溫誘導的ACD組大鼠與正常對照組比較,尿動力學檢查的各項參數(shù)均顯示出異常,逼尿肌肌條收縮幅度明顯降低,平滑肌收縮相關蛋白α-SMA,Calponin和SM-MHC在mRNA及蛋白水平的表達均明顯減少(P0.01)。通過膀胱壁注射BM-MSCs治療后,能夠在一定程度上修復受損的逼尿肌,提高逼尿肌收縮力,并且使平滑肌收縮相關蛋白α-SMA,Calponin和SM-MHC的表達水平部分地恢復(P0.01)。在額外加用丁酸鈉治療后,這些作用效果都有所增強。除此之外,丁酸鈉能夠促使BM-MSCs分化為平滑肌細胞,進而修復逼尿肌肌層。四、結論:BM-MSCs聯(lián)合丁酸鈉通過膀胱壁注射修復受損的膀胱壁并重建膀胱肌肉組織可能是應對ACD的一種新的治療策略。
[Abstract]:Objective: to investigate the possibility of sodium butyrate combined with rat bone marrow mesenchymal stem cells (BMSCs) in the treatment of detrusor myasthenia induced by frostbite by intravesical injection of sodium butyrate and rat bone marrow mesenchymal stem cells (BM-MSCs) to improve detrusor weakness by intravesical injection of sodium butyrate and bone marrow mesenchymal stem cells (BMSCs) in the rat model of detrusorrhagia induced by frostbite. Materials and methods Eighty-five female rats with Sprague-Dawley (SD) were divided into 5 groups with 17 rats in each group. A hypothermic model of bladder detrusor myasthenia was established in 68 rats. After the establishment of the model, Immediately, 0.2 ml of 0.2ml phosphate buffer saline containing 3 脳 10 6 M sodium butyrate (3 脳 10 6 M sodium butyrate) and 0.2 ml of PBS containing 1 脳 10 6 rat bone marrow mesenchymal stem cells (BM-MSCs) were injected into the bladder wall of each group, and the PBS containing 3 脳 106M sodium butyrate and 1 脳 106 rat bone marrow mesenchymal stem cells (BMSCs) were injected into the bladder wall of each group. The remaining 17 untreated rats were used as normal control group for 14 days to detect bladder urination function and detrusor contractility. The expression of 偽 -SMA-Calponin and SM-MHCs were detected by HE staining and Western blot. Results: compared with the normal control group, the parameters of urodynamic examination in hypothermia induced ACD rats were abnormal, and the contraction amplitude of detrusor strips was significantly decreased. The expression of 偽 -SMA-Calponin and SM-MHC in the level of mRNA and protein decreased significantly. After BM-MSCs was injected into the bladder wall, the damaged detrusor could be repaired to a certain extent, the contractile force of detrusor was increased, and the expression of 偽 -SMA-Calponin and SM-MHC was partly restored to P0.01. These effects were enhanced after the addition of sodium butyrate. In addition, sodium butyrate can induce BM-MSCs to differentiate into smooth muscle cells and repair the detrusor muscle layer. Conclusion: BM-MSCs combined with sodium butyrate may be a new treatment strategy to repair the damaged bladder wall and reconstruct the bladder muscle tissue through the injection of sodium butyrate into the bladder wall.
【學位授予單位】：第三軍醫(yī)大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R694.5

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