CAJ | 학술논문

目的探讨异氟醚预处理对大鼠局灶性脑缺血再灌注时5脂氧合酶(5-LOX)表达的影响.方法雄性成年SD大鼠39只,体重250 ～ 300 g,采用随机数字表法,将大鼠随机分为3组(n=13):假手术组(S组)、局灶性脑缺血再灌注组(I/R组)和异氟醚预处理组(I组).采用大脑中动脉阻断法制备大鼠局灶性脑缺血再灌注模型.I组吸入2％异氟醚2h,24 h后制备模型.再灌注24 h时进行神经功能缺陷评分,随后处死,取脑组织测量脑梗死体积,分别采用Western blot法和RT-PCR法测定5-LOX、髓样分化因子88 (MyD88)和NF-κB蛋白及其mRNA的表达水平.结果与S组比较,I/R组和l组神经功能缺陷评分升高,脑梗死体积增大,I/R组5-LOX、MyD88和NF-κB蛋白及其mRNA表达上调,I组5-LOX mRNA 、MyD88蛋白及其mRNA表达上调(P＜0.05)；与I/R组比较,I组神经功能缺陷评分降低,脑梗死体积减小,5-LOX、MyD88和NF-κB蛋白及其mRNA表达下调(P＜0.05).结论异氟醚预处理可能通过下调5-LOX表达,抑制MyD88/NF-κB信号通路,从而减轻大鼠局灶性脑缺血再灌注损伤.
목적 탐토이불미예처리대대서국조성뇌결혈재관주시5지양합매(5-LOX)표체적영향.방법 웅성성년SD대서39지,체중250 ～ 300 g,채용수궤수자표법,장대서수궤분위3조(n=13):가수술조(S조)、국조성뇌결혈재관주조(I/R조)화이불미예처리조(I조).채용대뇌중동맥조단법제비대서국조성뇌결혈재관주모형.I조흡입2％이불미2h,24 h후제비모형.재관주24 h시진행신경공능결함평분,수후처사,취뇌조직측량뇌경사체적,분별채용Western blot법화RT-PCR법측정5-LOX、수양분화인자88 (MyD88)화NF-κB단백급기mRNA적표체수평.결과 여S조비교,I/R조화l조신경공능결함평분승고,뇌경사체적증대,I/R조5-LOX、MyD88화NF-κB단백급기mRNA표체상조,I조5-LOX mRNA 、MyD88단백급기mRNA표체상조(P＜0.05)；여I/R조비교,I조신경공능결함평분강저,뇌경사체적감소,5-LOX、MyD88화NF-κB단백급기mRNA표체하조(P＜0.05).결론 이불미예처리가능통과하조5-LOX표체,억제MyD88/NF-κB신호통로,종이감경대서국조성뇌결혈재관주손상.
Objective To investigate the effect of isoflurane preconditioning on the expression of 5-lipoxy-genase (5-LOX) during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-nine male adult Sprague-Dawley rats weighing 250-300 g were randomly divided into 3 groups (n =13 each):sham operation group (group S); focal cerebral I/R group (group I/R); isoflurane preconditioning group (group Ⅰ).Focal cerebral I/R was produced by mid-cerebral artery occlusion in anesthetized rats.The rats inhaled 2 h of 2％ isoflurane and focal cerebral I/R was produced 24 h later in group I.The neurological deficits were scored at 24 h of reperfusion.The animals were then sacrificed.The brains were immediately removed for determination of the infarct size.The expression of 5-LOX,myeloid differentiation factor88 (MyD88) and nuclear factor kappa B (NF-κB) protein and mRNA was detected using Western blot and RT-PCR respectively.Results Compared with group S,the neurological deficit score was significantly increased,the infarct size was enlarged in groups I/R and I,the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was up-regulated in group I/R,and the expression of 5-LOX mRNA and MyD88 protein and mRNA was up-regulated in group I (P ＜ 0.05).Compared with group I/R,the neurological deficit score was significantly lower,the infarct size was smaller,and the expression of 5-LOX,MyD88 and NF-κB protein and mRNA was lower in group I (P ＜ 0.05).Conclusion Isoflurane preconditioning can reduce focal cerebral I/R injury by down-regulating the expression of 5-LOX and inhibiting MyD88/NF-κB signaling pathway in rats.