丁酸钠结合大鼠骨髓间充质干细胞改善大鼠逼尿肌无力的研究

发布时间：2018-05-04 18:39

本文选题：逼尿肌无力 + 骨髓间充质干细胞　；参考：《第三军医大学》2015年硕士论文

【摘要】：一、目的:探讨在冻伤引起的逼尿肌无力(acontractile detrusor,ACD)大鼠模型中,丁酸钠(Sodium Butyrate)联合大鼠骨髓间充质干细胞(rat bone marrow-derived mesenchymal stem cells,BM-MSCs)通过膀胱壁注射法改善逼尿肌无力的可能性。二、材料与方法:85只(Sprague-Dawley,SD)雌性大鼠,分为5组,每组17只。用68只大鼠建立低温诱导的膀胱逼尿肌无力(acontractile detrusor,ACD)模型。模型建立完成后,分别立即将0.2ml磷酸盐缓冲盐水(phosphate-buffered saline,PBS),0.2ml含有3×106 M丁酸钠(Sodium Butyrate)的PBS,0.2ml含有1×106大鼠骨髓间充质干细胞(BM-MSCs)的PBS,0.2ml含有3×106 M丁酸钠及1×106大鼠骨髓间充质干细胞的PBS注入各组大鼠膀胱壁内,剩余17只未处理大鼠作为正常对照组。14天后检测各组大鼠膀胱排尿功能,逼尿肌肌条收缩力,各组大鼠膀胱壁组织学改变情况用HE染色检测,RT-PCR及Western blot检测平滑肌收缩相关蛋白(α-SMA、Calponin和SM-MHC)的表达情况。三、结果:低温诱导的ACD组大鼠与正常对照组比较,尿动力学检查的各项参数均显示出异常,逼尿肌肌条收缩幅度明显降低,平滑肌收缩相关蛋白α-SMA,Calponin和SM-MHC在mRNA及蛋白水平的表达均明显减少(P0.01)。通过膀胱壁注射BM-MSCs治疗后,能够在一定程度上修复受损的逼尿肌,提高逼尿肌收缩力,并且使平滑肌收缩相关蛋白α-SMA,Calponin和SM-MHC的表达水平部分地恢复(P0.01)。在额外加用丁酸钠治疗后,这些作用效果都有所增强。除此之外,丁酸钠能够促使BM-MSCs分化为平滑肌细胞,进而修复逼尿肌肌层。四、结论:BM-MSCs联合丁酸钠通过膀胱壁注射修复受损的膀胱壁并重建膀胱肌肉组织可能是应对ACD的一种新的治疗策略。
[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 伪 -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 伪 -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 伪 -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.
【学位授予单位】：第三军医大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R694.5

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