CAJ | 학술논문

目的：观察特异性激活Toll样受体3（Toll‐like receptor 3，TLR3）‐Toll／IL‐1受体结构域接头分子（Toll／IL‐1 receptor domain containing adaptor inducing IFN‐β，TRIF）信号通路药物聚肌胞苷酸（polyinosinic polycytidylic acid ，Poly I：C）对局灶性脑缺血损伤小鼠是否有保护作用，并探讨保护作用是否与抑制炎性作用有关。方法对小鼠进行一次性肌肉注射0.3 mg／kg Poly I：C ，24 h后进行左侧大脑中动脉栓塞（middle cerebral artery occlusion ，MCAO），栓塞2 h后进行再灌注6、12、22 h ，诱导小鼠的脑缺血再灌注损伤模型，T TC染色方法测定脑缺血体积；Western blot方法检测缺血侧脑组织TRIF蛋白表达；ELISA方法检测小鼠缺血侧半脑脑组织炎性因子干扰素‐β（interferon‐β，IFN‐β）、白细胞介素‐10（interleukin‐10，IL‐10）、白细胞介素‐6（interleukin‐6，IL‐6）、肿瘤坏死因子‐α（tumor necrosis factor‐α，TNF‐α）的含量。结果缺血2 h再灌注6、12、22 h的小鼠出现明显的神经缺陷症状及脑组织梗死，在缺血再灌注各个时间点，小鼠缺血侧脑组织中IL‐6、TNF‐α表达均升高。0.3 mg／kg Poly I：C能减少梗死面积，改善神经缺陷，提高小鼠缺血侧脑组织 TRIF蛋白的表达，能在不同时间点升高IFN‐β水平并降低缺血再灌注缺血侧脑组织IL‐6和 TNF‐α的含量。结论0.3 mg／kg Poly I：C对脑缺血损伤小鼠有保护作用，保护作用机制与抑制小鼠脑缺血再灌注损伤过程中的炎症反应有关。
목적：관찰특이성격활Toll양수체3（Toll‐like receptor 3，TLR3）‐Toll／IL‐1수체결구역접두분자（Toll／IL‐1 receptor domain containing adaptor inducing IFN‐β，TRIF）신호통로약물취기포감산（polyinosinic polycytidylic acid ，Poly I：C）대국조성뇌결혈손상소서시부유보호작용，병탐토보호작용시부여억제염성작용유관。방법대소서진행일차성기육주사0.3 mg／kg Poly I：C ，24 h후진행좌측대뇌중동맥전새（middle cerebral artery occlusion ，MCAO），전새2 h후진행재관주6、12、22 h ，유도소서적뇌결혈재관주손상모형，T TC염색방법측정뇌결혈체적；Western blot방법검측결혈측뇌조직TRIF단백표체；ELISA방법검측소서결혈측반뇌뇌조직염성인자간우소‐β（interferon‐β，IFN‐β）、백세포개소‐10（interleukin‐10，IL‐10）、백세포개소‐6（interleukin‐6，IL‐6）、종류배사인자‐α（tumor necrosis factor‐α，TNF‐α）적함량。결과결혈2 h재관주6、12、22 h적소서출현명현적신경결함증상급뇌조직경사，재결혈재관주각개시간점，소서결혈측뇌조직중IL‐6、TNF‐α표체균승고。0.3 mg／kg Poly I：C능감소경사면적，개선신경결함，제고소서결혈측뇌조직 TRIF단백적표체，능재불동시간점승고IFN‐β수평병강저결혈재관주결혈측뇌조직IL‐6화 TNF‐α적함량。결론0.3 mg／kg Poly I：C대뇌결혈손상소서유보호작용，보호작용궤제여억제소서뇌결혈재관주손상과정중적염증반응유관。
Objective To examine the influence of polyinosinic‐polycytidylic acid(Poly I:C)on focal cerebral ischemia‐reper‐fusion injury through Toll‐like receptor 3(TLR3)‐Toll/IL‐1 receptor domain‐containing adaptor inducing IFN‐β(TRIF)signa‐ling pathway in mice and to explore the effects of Poly I:C on the inhibition of inflammatory reaction.Methods Mouse ischemi‐a/reperfusion(I/R)models were established by 2 h left middle cerebral artery occlusion(MCAO)followed by 6 ,12 ,22 h reperfu‐sion.Animals were treated with 0.3 mg/kg Poly I:C via one‐time intramuscular injection before MCAO.Cerebral infarct volume was detected by TTC staining ;the expression level of TRIF protein in ischemic brain tissues was measured by Western blot ,and TNF‐α,IL‐6 ,IFN‐β,and IL‐10 levels by ELISA.Results Two‐h left MCAO followed by 6 ,12 ,22 h reperfusion could result in severe nerve defects and cerebral infarction.The levels of TNF‐αand IL‐6 were significantly increased in ischemic brain tissues at each I/R time point.Treatment of the mice with Poly I:C(0.3 mg/kg)prior to MCAO could reduce cerebral infarct volume , improve the nerve defects ,increase TRIF protein expression ,enhance the secretion of IFN‐β,and down‐regulate the levels of TNF‐αand IL‐6 in ischemic brain tissues.Conclusion Poly I:C can protect against cerebral ischemia‐reperfusion injury by re‐ducing inflammation reaction.