大鼠全脑缺血/再灌注后TLR3mRNA与IL-6mRNA的表达及其相关性

目的 观察大鼠全脑缺血/再灌注（I/R）后海马Toll样受体3（TLR3）mRNA与白细胞介素-6（IL-6）mRNA的表达并分析其相关性,探讨TLR3在大鼠脑I/R损伤中的作用.方法 将SD大鼠随机分为假手术组（sham组）和I/R组,采用Pulsinelli-Brierley 4动脉阻断方法制作大鼠全脑I/R损伤模型,在全脑缺血15 min后,分别再灌注6、12、24、48、72、96 h,采用RT-PCR方法检测不同时间点海马TLR3 mRNA与IL-6 mRNA的表达情况并做相关性分析.结果 与sham组相比,大鼠全脑I/R 12 h,海马TLR3 mRNA与IL-6 mRNA表达均开始增加,72 h达到高峰,96 h下降,仍高于sham组（P〈0.01）,6 h时与sham组比较差异无统计学意义（P〉0.05）.TLR3 mRNA与IL-6 mRNA的表达呈正相关（r=0.959,P〈0.01）.结论 大鼠脑I/R后TLR3 mRNA表达上调,可能通过促使炎性细胞因子的分泌介导脑I/R炎性损伤.

Correlation between the expressions of TLR3 mRNA and IL-6 mRNA following global cerebral ischemia/reperfusion injury in rats

Objective To observe the expressions of Toll - like receptor 3 （TLR3） mRNA and IL - 6 mRNA in the hippocampus following global cerebral ischemia/reperfusion （I/R） injury in rats and to analyze their correlation in order to explore the role of TLR3 in the cerebral I/R injury. Methods The SD rats were randomized into sham - operated group and I/R group. The model of global brain UR was established by Pulsinelli - Brierley four - vessel occlusion in SD rats. 15 rain after the cerebral ischemia, the reperfusion was performed at 6 h, 12 h, 24 h, 48 h, 72 h and 96 h, respec- tively. The mRNA expressions of TLR3 and IL - 6 in the hippocampus following I/R were detected by RT - PCR at each time point. Moreover, the correlation between TLR3 mRNA and IL - 6 mRNA expressions was analyzed. Results Compared with shamoperated group, the mRNA expression levels of both TLR3 and IL -6 began to increase at 12 h and reached a peak at 72 h and then gradually declined and were still higher than sham - operated group at 96 h after cerebral I/R （ P 〈 0.05 ） but differences had no statistical significance at 6 h （ P 〉 0.05 ）. The mRNA expression of TLR3 was positively correlated with the expression mRNA of IL- 6 （r = 0. 959, P 〈 0.01 ）. Conclusion The mRNA expression of TLR3 in the hippocampus is upregulated following global cerebral I/R, which might mediate cerebral I/R inflammatory injury via the secretion of inflammatory factor.