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作 者:边晓慧[1,2] 赵桂锋[3] 孙立[1] 刘娜[4] 李德天[2] 冯江敏[1]
机构地区:[1]中国医科大学附属第一医院肾内科,沈阳110001 [2]中国医科大学附属盛京医院肾内科,沈阳110004 [3]中国医科大学附属盛京医院先天畸形研究中心实验室,沈阳110004 [4]内蒙古鄂尔多斯市中心医院肾内科,内蒙古鄂尔多斯017000
出 处:《中国医科大学学报》2014年第2期131-135,共5页Journal of China Medical University
基 金:辽宁省自然科学基金(20072095);辽宁省社会发展攻关计划(201225094)
摘 要:目的观察骨髓间充质干细胞(MSC)延缓肾纤维化的能力以及可能的机制。方法建立SD大鼠5/6肾切除残肾模型,尾静脉注射绿色荧光蛋白标记的MSC,移植后4周观察肾功能以及肾脏病理的改变,应用免疫组化和免疫印迹方法观察残肾组织中CD44、CD68、TGF-β1和α-SMA的表达。结果 MSC能够改善残肾功能和延缓肾纤维化;MSC不仅减少了巨噬细胞的浸润和肌成纤维细胞的堆积,而且抑制了CD44和TGF-β1的表达。结论 MSC治疗能够延缓肾纤维化,其主要机制可能与其抗炎作用和免疫抑制有关。Objective To investigate the role of mesenchymal stem cells (MSC) therapy in renal frbrosis and explore the mechanism. Methods Remnant kidney model was established by 5/6 nephrectomy in Sprague-Dawley rats, and the animals received MSC treatment via tail vein injection. Renal function and histological analysis were performed 4 weeks after cell transplantation. Immunohistochemistry and Western blot were used to de- tect the expression of CD44, CD68, TGF- β1 and α - SMA. Results The functional benefits of MSC treatment were demonstrated by improved clini- cal signs and reduced fibrosis formation. The infiltration of macrophages and the accumulation of myofibroblasts were reduced after MSC treatment. The levels of TGF-β1 and CD44 were also decreased in MSC treated groups. Conclusion MSC therapy can attenuate fibrosis progression in rem- nant kidney model. Moreover, the anti-inflammatory and immunosuppressive potential of MSC may be involved in the decreased fibrosis in kidney.
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