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目的:观察大鼠肾缺血再灌注后Toll样受体4(Toll-like receptors 4,TLR4)和细胞核因子kappa B(Nuclear factorkappa B,NF-κB)p50蛋白的表达情况,探讨它们参与肾缺血再灌注损伤的作用机理。方法:SD雄性大鼠48只随机分为对照组(Control组,简称C组)、缺血再灌注组(Ischemia-reperfusion组,简称Ir组)2个实验组,每组各4个时相(6、12、24、72 h)。采用切除右肾,夹闭左肾动脉45 min后恢复灌流建立肾缺血再灌注损伤模型。免疫组化二步法检测大鼠肾组织中TLR4和NF-κBp50蛋白的表达情况,测定髓过氧化物酶(Myeloperoxidase,Mpo)活性及血清肌酐(Serum creatinine,Scr)水平以反映中性粒细胞活化及肾功能损害的程度。结果:TLR4和NF-κBp50蛋白在C组中几乎无表达,Ir组中表达明显增强(P<0.01)。与C组比较,Ir组Scr水平明显升高,Mpo活性显著增加(P<0.01)。结论:肾缺血再灌注损伤的发生可能与TLR4活化NF-κB诱导的炎症反应有关。
OBJECTIVE: To observe the expression of p50 protein of Toll-like receptors 4 (TLR4) and nuclear factor kappa B (NF-κB) after renal ischemia-reperfusion in rats, Mechanism of blood reperfusion injury. Methods: Forty-eight SD male rats were randomly divided into control group (C group), ischemia-reperfusion group (Ir group) and experimental group 6, 12, 24, 72 h). The right kidney was excised and the left renal artery was closed for 45 min before reperfusion to establish a model of renal ischemia-reperfusion injury. Immunohistochemistry was used to detect the expression of TLR4 and NF-κB p50 in rat renal tissue. The activity of Myeloperoxidase (Mpo) and Serum creatinine (Scr) were measured to reflect the expression of neutrophil Activated and renal damage extent. Results: The expressions of TLR4 and NF-κBp50 protein were almost not seen in group C, but significantly increased in group Ir (P <0.01). Compared with group C, the level of Scr in Ir group was significantly increased and Mpo activity was significantly increased (P <0.01). Conclusion: The occurrence of renal ischemia-reperfusion injury may be related to the activation of NF-κB induced by TLR4.