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目的采用颈交感干离断(TCST)模拟星状神经节阻滞,观察其对局灶性脑缺血再灌注损伤(CIRI)大鼠脑梗死容积及海马诱导型一氧化氮合酶(iNOS)表达等的影响,并探讨其脑保护作用的机制。方法将大鼠随机分成实验组(A组)、对照组(B组)和假手术组(C组);采用线栓法行大脑中动脉栓塞(MCAO)制作大鼠局灶性CIRI模型,A组于TCST后即行MCAO,2h后再恢复灌注;B组为单纯CIRI组;C组仅完成与A组相似的手术步骤但不造成MCAO、不行TCST;再灌注24h后观察各组大鼠神经行为学评分、脑梗死容积及海马iNOS的表达变化。结果A组大鼠脑梗死容积和神经行为学评分均低于B组(P<0.05);与A组、C组相比,B组大鼠海马iNOS的表达增加(P<0.05),而A组与C组间无显著差异(P>0.05)。结论TCST可通过下调大鼠海马iNOS的表达而对局灶性CIRI发挥脑保护作用。
Objective To investigate the effect of trichostatin on the infarct volume and the expression of iNOS in focal cerebral ischemia-reperfusion injury (CIRI) rats by simulating stellate ganglion block by cervical sympathetic dry off (TCST) Expression and other effects, and explore its mechanism of brain protection. Methods The rats were randomly divided into experimental group (A group), control group (B group) and sham operation group (C group). The focal CIRI model was established by middle cerebral artery occlusion (MCAO) The rats in group were given MCAO after TCST, and then reperfused after 2 hours. Group B was treated with CIRI alone. Group C only completed similar surgical procedures with group A but did not cause MCAO or TCST. After 24 hours of reperfusion, the neurological behaviors of rats in each group were observed Scoring, cerebral infarction volume and the expression of iNOS in hippocampus. Results Compared with group A and group C, the volume of cerebral infarction and neurological behavior in group A were significantly lower than that in group B (P <0.05), and the expression of iNOS in group B was increased (P <0.05) There was no significant difference between group C and C (P> 0.05). Conclusion TCST can exert cerebral protective effect on focal CIRI by down-regulating the expression of iNOS in hippocampus of rats.