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目的探讨TOLL样受体4(TLR4)在脑缺血再灌注中的保护作用。方法C3H/HeJ小鼠16只采用线栓法制作TLR4先天缺损大脑中动脉缺血再灌注模型(C3H/HeJ组),以C3H/HeN小鼠16只作对照(C3H/HeN组),观察缺血6h及再灌注24h时,两组小鼠神经功能缺损评分、脑含水量、脑梗死体积及血清TNF-α水平。光镜及电镜观察两者缺血再灌注脑组织损伤情况。结果与C3H/HeN组比较,再灌注24h时,C3H/HeJ组小鼠的神经功能缺损评分明显减小(P<0.05);脑含水量明显降低,脑梗死体积显著缩小(P<0.01);血清中TNF-α浓度明显降低(P<0.05);脑缺血皮质区的神经细胞超微结构改变轻于C3H/HeN组小鼠。结论C3H/HeJ小鼠脑缺血再灌注损伤明显减轻,TLR4介导了脑缺血再灌注损伤。其机制可能与炎性细胞因子减少有关。
Objective To investigate the protective effect of Toll-like receptor 4 (TLR4) on cerebral ischemia-reperfusion. Methods Sixteen C3H / HeJ mice were randomly divided into three groups: control group (C3H / HeJ group), control group (C3H / HeN group) Blood 6h and 24h reperfusion, two groups of mice neurological deficit score, brain water content, cerebral infarction volume and serum TNF-α levels. Light and electron microscopy were used to observe the damage of both brain tissue after ischemia and reperfusion. Results Compared with C3H / HeN group, the neurological deficit score of C3H / HeJ group was significantly decreased at 24 hours after reperfusion (P <0.05); the water content of brain decreased significantly and the volume of cerebral infarction was significantly reduced (P <0.01). The concentration of TNF-α in serum decreased significantly (P <0.05). The ultrastructure changes of neurons in cortex of ischemic area were lighter than that of C3H / HeN mice. Conclusion The cerebral ischemia-reperfusion injury in C3H / HeJ mice was significantly reduced, TLR4 mediated cerebral ischemia-reperfusion injury. The mechanism may be related to the reduction of inflammatory cytokines.