CAJ | 학술논문

目的：观察疏血通注射液（SXT）对局灶性脑梗死大鼠缺血周围区细胞凋亡和 Toll样受体4（TLR4）表达的影响，探讨SXT对缺血脑损伤的神经保护机制。方法：采用线栓法制作SD大鼠大脑中动脉闭塞模型（MCAO ），随机分为3组：假手术组、模型组、SXT治疗组；分别在缺血12、24、48 h及72 h采用DNA原位末端缺口标记法（TUNEL）、逆转录聚合酶链反应（RT-PCR）和免疫组化法检测缺血周围区神经细胞凋亡、TLR4 mRNA和蛋白表达。结果在模型组中，TUNEL阳性细胞数、TLR4 mRNA和蛋白表达在缺血12 h逐渐增加，24 h达到峰值后表达有所下降，较假手术组仍维持高位表达（P＜0．01）；在SXT治疗组中，上述表达在缺血24 h后均较模型组降低（P＜0．05），并随着治疗时间延长呈下降趋势（P＜0．05）。结论：在脑缺血损伤亚急性期，细胞凋亡与TLR4表达有关，SXT能抑制细胞凋亡，下调缺血周围区 TLR4表达，这可能是其发挥神经保护作用的机制之一。
목적：관찰소혈통주사액（SXT）대국조성뇌경사대서결혈주위구세포조망화 Toll양수체4（TLR4）표체적영향，탐토SXT대결혈뇌손상적신경보호궤제。방법：채용선전법제작SD대서대뇌중동맥폐새모형（MCAO ），수궤분위3조：가수술조、모형조、SXT치료조；분별재결혈12、24、48 h급72 h채용DNA원위말단결구표기법（TUNEL）、역전록취합매련반응（RT-PCR）화면역조화법검측결혈주위구신경세포조망、TLR4 mRNA화단백표체。결과재모형조중，TUNEL양성세포수、TLR4 mRNA화단백표체재결혈12 h축점증가，24 h체도봉치후표체유소하강，교가수술조잉유지고위표체（P＜0．01）；재SXT치료조중，상술표체재결혈24 h후균교모형조강저（P＜0．05），병수착치료시간연장정하강추세（P＜0．05）。결론：재뇌결혈손상아급성기，세포조망여TLR4표체유관，SXT능억제세포조망，하조결혈주위구 TLR4표체，저가능시기발휘신경보호작용적궤제지일。
Objective To investigate the effects of Shuxuetong Injection (SXT ) on expressions of cell apoptosis and TLR4 a-round ischemic area after focal cerebral infarction in rats and to discuss its neuroprotective mechanism on ischemia-induced brain in-jury .Methods The SD rats were subjected to establish the model of middle cerebral artery occlusion (MCAO)by nylon monofila-ment suture ,then were randomly divided into the sham-operated group ,the model group and the SXT treatment group ;the cell ap-optosis and the expressions of TLR4 mRNA and protein around ischemic area at 12 ,24 ,48 ,72 h after cerebral ischemia were detec-ted respectively by TUNEL test mediated with DNA ,RT-PCR and immunohistochemistry .Results In the model group ,the number of TUNEL positive cells ,the expressions of TLR4 mRNA and protein were gradually increased at 12 h ,reached the peak at 24 h , then decreased and were still higher than those in the sham-operated group(P<0 .01);in the SXT treatment group ,these expres-sions after 24 h were lower than those in the model group (P<0 .05)and declined as the treatment time increase(P<0 .05) .Conclu-sion In subacute stage of cerebral ischemia injury ,apoptosis is related with the expression of TLR4 ,SXT may inhibit apoptosis , down-regulate the expression of TLR4 around ischemic area ,this may be one of the mechanisms of neuroprotection .