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目的:探讨骨髓间充质干细胞(BMSCs)促肾缺血-再灌注损伤修复的能力及机制。方法:取健康3周龄C57BL/6J小鼠的骨髓细胞悬液,进行BMSCs体外扩增培养。将8周龄C57BL/6J小鼠随机分为假手术组(10只)、平行对照组(10只)和细胞移植组(28只)。建立肾缺血-再灌注损伤模型,将BMSCs移植到细胞移植组小鼠中,平行对照组注射生理盐水。通过检测肾功能观察BMSCs对肾损伤的促修复作用。并通过检测氧化应激指标和观察蓝色荧光标记供体BMSCs在受体内的踪迹,初步探讨BMSCs促宿主损伤肾组织修复的机制。结果:分离培养的BMSCs增殖旺盛,纯度较高,且均质性和稳定性好。平行对照组表现为小鼠整体状态差,肾功能指标和氧化应激指标都没有得到改观。细胞移植组小鼠整体状态良好,肾功能指标和氧化应激指标明显改善(P<0.05)。并在宿主恢复的肾组织中发现了较多的带有蓝色荧光的细胞存在。结论:BMSCs在体外易分离培养,具有旺盛的增殖能力;移植BMSCs后,具有向受损组织归巢的作用,并参与和提高肾缺血-再灌注损伤后宿主C57BL/6J小鼠的恢复。
Objective: To investigate the ability and mechanism of bone marrow mesenchymal stem cells (BMSCs) for promoting renal ischemia-reperfusion injury. Methods: Bone marrow cell suspension from healthy 3-week-old C57BL / 6J mice was used to expand and culture BMSCs. Eight-week-old C57BL / 6J mice were randomly divided into sham operation group (n = 10), parallel control group (n = 10) and cell transplantation group (n = 28). The model of renal ischemia-reperfusion injury was established. The BMSCs were transplanted into the cell transplantation group, and the parallel control group was injected with normal saline. BMSCs were observed to promote renal repair by detecting renal function. And through the detection of oxidative stress indicators and observation of blue fluorescent labeled donor BMSCs traces in the receptor, to explore the mechanism of BMSCs promote primary injury of renal tissue repair. Results: BMSCs isolated and cultured had strong proliferation, high purity and good homogeneity and stability. Parallel control group showed poor overall state of mice, kidney function indicators and indicators of oxidative stress have not been changed. The mice in the cell transplantation group had a good overall condition with significantly improved renal function and oxidative stress (P <0.05). And found more cells with blue fluorescence in the host-recovered kidney tissue. CONCLUSION: BMSCs are easily isolated and cultured in vitro and have strong proliferative capacity. After transplanted with BMSCs, they can homing to damaged tissues and participate in and improve the recovery of host C57BL / 6J mice after renal ischemia-reperfusion injury.