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目的观察Toll样受体4(TLR4)和肿瘤坏死因子-α(TNF-α)的表达变化,探讨缺血预处理对大鼠脑缺血再灌注损伤的保护作用。方法 36只SPF级健康雄性SD大鼠随机分为缺血预处理组(CIP组)、缺血再灌注组(I/R组)和假手术组(Sham组)各12只;I/R组采用线栓法阻断大脑中动脉(MCAO)2h建立模型,CIP组先给予MCAO阻断10min,再灌注72h后给予与I/R组相同的处理,假手术组仅分离血管。均于术后1d取材,TTC染色法检测脑梗死体积,Zea Longa评分标准对神经功能评分,荧光实时定量PCR(Real-time Quantitative polymerase chain reaction)法测定TLR4和TNF-α mRNA 表达水平。结果缺血再灌注1d后,CIP组大鼠脑梗死体积、神经功能缺损评分明显低于I/R组,差异有显著统计学意义(P<0.05);TLR4、TNF-α mRNA CIP组与I/R组表达水平明显高于Sham组,差异有显著统计学意义(P<0.05,P<0.01),CIP组表达水平明显低于I/R组(P<0.05)。结论缺血预处理能改善由再灌注损伤引起的脑损伤与功能障碍,可能与下调促炎因子的表达、减轻炎症反应有关。
Objective To observe the expression changes of Toll-like receptor 4 (TLR4) and tumor necrosis factor-α (TNF-α) and to explore the protective effect of ischemic preconditioning on cerebral ischemia-reperfusion injury in rats. Methods Thirty-six SPF healthy male Sprague-Dawley rats were randomly divided into ischemia preconditioning group (CIP group), ischemia / reperfusion group (I / R group) and sham operation group (Sham group) The MCAO model was established by occlusion of the middle cerebral artery (MCAO) by the suture occlusion method. The CIP group was given MCAO for 10 minutes and then the same treatment as the I / R group 72 hours after the reperfusion. Only the blood vessels were separated from the sham operation group. All the rats were sacrificed at 1 day after operation. The volume of cerebral infarction was detected by TTC staining, the neurological function was assessed by Zea Longa score, and the mRNA expression of TLR4 and TNF-α by real-time quantitative polymerase chain reaction. Results Compared with I / R group, the volume of cerebral infarction and the neurological deficit score of CIP group were significantly lower than that of I / R group (P <0.05), and the level of TLR4, TNF-α mRNA CIP and I / R group was significantly higher than Sham group, the difference was statistically significant (P <0.05, P <0.01), CIP group was significantly lower than the I / R group (P <0.05). Conclusion Ischemic preconditioning can improve brain injury and dysfunction caused by reperfusion injury, which may be related to the downregulation of proinflammatory cytokines and the reduction of inflammatory reaction.