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目的观察三维(3-D)球体间充质干细胞(MSCs)移植对脑缺血再灌注损伤大鼠脑组织肿瘤坏死因子α(TNF-α)及凋亡相关蛋白表达的影响,探讨3-D球体MSCs的神经保护作用及可能机制。方法实验大鼠随机分为假手术组、溶剂对照组、3-D球体MSCs治疗组(n=36),假手术组常规分离大脑中动脉(MCA)但不结扎,MSCs治疗组采用线栓法建立大脑中动脉缺血(MCAO)模型后给予MSCs移植,溶剂对照组模型建立成功后给予等体积溶剂对照。各组大鼠分别于移植治疗后1、3、7d进行神经功能评分;采用ELISA和RT-PCR方法检测大鼠脑组织中的TNF-α表达;采用免疫组化SABC法染色,观察损伤侧大鼠脑组织Caspase-3和Caspase-8蛋白的表达。结果与假手术组、溶剂对照组相比,MSCs治疗组大鼠神经运动功能评分降低(P<0.05);与假手术组相比,溶剂对照组大鼠脑组织TNF-α、Caspase-3和Caspase-8表达增加(P<0.01);与溶剂对照组相比,MSCs治疗组脑组织TNF-α、Caspase-3、Caspase-8表达下降(P<0.05,P<0.01)。结论 3-D球体MSCs移植可能通过下调脑组织中炎性因子TNF-α含量及减少凋亡相关蛋白的表达,改善大鼠脑缺血再灌注损伤后神经运动功能。
Objective To observe the effect of 3-D MSCs transplantation on the expression of tumor necrosis factor-α (TNF-α) and apoptosis-related protein in brain tissue of rats with cerebral ischemia-reperfusion injury and to explore the role of 3-D Neuroprotective Effect of Sphere MSCs and Its Possible Mechanism. Methods The experimental rats were randomly divided into sham operation group, solvent control group and 3-D spherical MSCs treatment group (n = 36). Rats in sham operation group were given normal MCA but not ligation. MSCs were transplanted after establishment of middle cerebral artery occlusion (MCAO) model. The solvent control group model was established after successful administration of equal volume of solvent control. Neurological scores were evaluated at 1, 3 and 7 days after transplantation. The expression of TNF-α in rat brain was detected by ELISA and RT-PCR. The expression of TNF-α was detected by immunohistochemical SABC staining. Expression of Caspase-3 and Caspase-8 in Brain Tissue of Rats. Results Compared with the sham operation group and the solvent control group, the scores of neuromotor function in the MSCs-treated rats decreased (P <0.05). Compared with the sham operation group, the levels of TNF-α, Caspase-3 and Compared with the solvent control group, the expression of Caspase-8 and Caspase-8 decreased (P <0.05, P <0.01) in the MSCs treated group. Conclusions 3-D spherical MSCs transplantation may improve neural motor function after cerebral ischemia-reperfusion injury in rats by down-regulating the expression of TNF-α and decreasing the expression of apoptosis-related protein.