缺血预处理对缺血再灌注损伤大鼠肾组织TLR2表达的影响

目的观察缺血预处理对缺血／再灌注损伤大鼠肾组织Toll样受体2（TLR2）表达的影响。方法将24只雄性SD大鼠随机分为3组：假手术对照组（SHAM组）、单纯缺血再灌注组（I／R组）和缺血预处理组（IPC组），每组8只。于术后24h留取各组大鼠血标本和肾组织。检测各组大鼠血肌酐（SCr）和尿素氮（BUN），肾组织切片行HE染色后观察其病理学改变，酶联免疫吸附法（ELISA）检测肾组织肿瘤坏死因子-α（TNF-α）含量，实时荧光定量多聚酶链反应检测肾组织TLR2mRNA表达，Westernblot检测肾组织TLR2蛋白表达。结果与SHAM组相比，I／R组大鼠SCr和BUN升高，肾组织TNF-α含量和TLR2蛋白表达升高，差异均有统计学意义（P〈0．01）；与I／R组相比，IPC组大鼠SCr和BUN降低，肾组织TNF-α含量和TLR2蛋白表达降低，差异均有统计学意义（P〈0．05）。结论缺血预处理可能通过抑制大鼠。肾组织TLR2表达及其信号通路，下调TNF-α的表达，发挥其肾脏保护作用。

The effects of ischemic preconditioning on the renal expression of toll-like receptor2 in ischemia-reperfusion injury rats

Objective To observe the effect of ischemic preconditioning on the renal expression of toll-like receptor2 （TLR2） in ischemia/reperfusion injury rats. Methods Twenty-four male SD rats were randomly divided into three groups： sham operation group （SHAM group）, isehemia/reperfu- sion group （I/R group）, ischemic preconditioning group （IPC group ）. Blood and kidneys were obtained at the 24th hour after surgery. Renal function was determined by measuring blood urea nitrogen and serum creatinine. Changes in renal morphology were observed by hematoxylin-eosine staining. En- zyme-linked immunosorbent assay was used to detect the expression of TNF-α in the kidney samples. Real-time fluorescence quantitative PCR method was used to examine the expression of TLR2 mRNA in the kidney samples. Western blot analysis was used to detect the protein expression of TLR2 in the kidney samples. Results The expression of TLR2 mRNA and protein, and TNF-α in renal tissues was remarkably up-regulated in I/R group as compared with that in SHAM group, as well as the content of serum creatinine （SCr） and blood urea nitrogen （BUN） （P〈0. 01）. As compared with that in I/R group, the expression of TLR2 mRNA and protein, and TNF-α in renal tissues was decreased significantly in IPC group, as well as the content of SCr and BUN （P〈0. 05）. Conclusion Ischemic precon-ditioning may protect kidneys by inhibiting the expression of TLR2 and its signaling pathway to reduce the expression of TNF-α.