【摘要】 目的观察骨髓间质干细胞（MSCs）对氯化汞（HgCl₂）导致的急性肾小管损伤有无治疗作用,并探讨其可能的机制。方法建立Hgcl₂腹腔注射导致大鼠急性肾衰竭模型。SD大鼠分为MSCs组（HgCl₂+MSCs）、生理盐水组（HgCl₂+生理盐水）及正常对照组。7 d后,观察体重、生存率、肾功能、肾脏病理改变,进行增殖细胞核抗原（PCNA）、巨噬细胞标志物ED-1和增强绿色荧光融合蛋白（EGFP）免疫组织化学染色,用RT-PCR技术检测肾组织内细胞因子的表达情况,并观察EGFP转基因的MSCs在肾脏的分布情况。结果MSCs组在体重、生存率、肾功能、肾脏病理改变上,均明显好于生理盐水组；肾组织内PCNA⁺及ED-1⁺细胞数明显少于生理盐水组；促进肾小管损伤修复的生长因子表皮生长因子（EGF）、血小板源生长因子（PDGF）、肝细胞生长因子（HGF）在肾组织内表达明显高于生理盐水组,而促炎症因子TNF-α则明显低于生理盐水组。7 d时,间质干细胞在肾间质中偶尔可见到,而肾小管中未见。结论MSCs输注可促进HgCl₂所致的急性肾小管损伤的修复,其作用机制可能是通过调节肾组织中细胞因子的分泌起作用,而非完全依靠转分化成肾小管上皮细胞。更多还原

【Abstract】 Objective To investigate whether mesenchymal stem cells can promote the recovery of acute renal tubular damage induced by mercuric chloride and to explore its possible mechanism.Methods Acute renal failure rat model was established by intraperitoneal injection of mercuric chloride.SD rats were randomly divided into three groups which were MSCs injection group, saline infusion group and normal control group.Seven days later,the changes of rat weight,survival,renal function and pathology were observed;PCNA,ED-1 and GFP were detected by immunohistochemistry; The expression of cytokines in kidney and the distribution of GFP plasmid-transfected MSCs in kidney were examined by RT-PCR.Results MSCs infusion ameliorated the decline of rat weight,survival, renal function,and pathological changes.PCNA and ED-1 positive cells in MSCs group were fewer than those in saline group.Expression of growth factors EGF,PDGF,HGF were obviously up- regulated and pre-inflammatory cytokines TNF-αwas significantly reduced in MSCs-treated kidneys. GFP-labelled MSCs occurred occasionally in renal interstitium of MSCs-treated rats,but not in renal tubules.Conclusions Bone marrow mesenchymal stem cells can promote the recovery of acute renal tubular epithelial cells damage caused by mercuric chloride.The mechanism may partly depend on regulating the excretion of cytokines in renal microenvironment rather than completely depend on their differentiation to tubular cells.更多还原