CAJ | 학술논문

目的探讨异氟醚后处理对缺血缺氧性脑损伤新生大鼠脑组织血管内皮生长因子(VEGF)表达的影响.方法出生后7d的SD大鼠156只,雌雄不拘,采用随机数字表法,将其分为3组(n=52):假手术组(S组)、缺血缺氧性脑损伤组(HIBI组)和异氟醚后处理组(Ⅰ组).采用结扎左颈总动脉+低氧(吸入8％湿化氧气-92％氮气)2 h的方法建立缺血缺氧性脑损伤模型.Ⅰ组于低氧2h时开始吸入1％异氟醚1h,HIBI组吸入30％氧气-70％氮气1h.S组仅做颈动脉分离,不制备模型,其余同HIBI组.于模型制备结束后1、2、3和7 d(T1-4)时,取受损侧脑组织,观察病理学结果,计数海马和皮层死亡神经元,分别采用免疫组化法和Western blot法测定VEGF的表达水平.于T2时测定脑梗死体积百分比.结果仅S组未见脑梗死发生;与S组比较,HIBI组和Ⅰ组T1-4时受损侧海马和皮层死亡神经元计数升高,VEGF表达上调(P＜0.05);与HIBI比较,Ⅰ组脑梗死体积百分比降低,T1.2时受损侧海马和皮层死亡神经元计数降低,VEGF表达上调(P＜0.05),S组各时点受损侧海马和皮层死亡神经元计数和VEGF表达比较差异无统计学意义(P＞0.05),HIBI组T3时、Ⅰ组T2时VEGF表达水平达高峰(P＜0.05).Ⅰ组受损侧脑组织病理学损伤较HIBI组减轻.结论异氟醚后处理可能通过上调脑组织VEGF表达,减轻新生大鼠缺血缺氧性脑损伤.
목적 탐토이불미후처리대결혈결양성뇌손상신생대서뇌조직혈관내피생장인자(VEGF)표체적영향.방법 출생후7d적SD대서156지,자웅불구,채용수궤수자표법,장기분위3조(n=52):가수술조(S조)、결혈결양성뇌손상조(HIBI조)화이불미후처리조(Ⅰ조).채용결찰좌경총동맥+저양(흡입8％습화양기-92％담기)2 h적방법건립결혈결양성뇌손상모형.Ⅰ조우저양2h시개시흡입1％이불미1h,HIBI조흡입30％양기-70％담기1h.S조부주경동맥분리,불제비모형,기여동HIBI조.우모형제비결속후1、2、3화7 d(T1-4)시,취수손측뇌조직,관찰병이학결과,계수해마화피층사망신경원,분별채용면역조화법화Western blot법측정VEGF적표체수평.우T2시측정뇌경사체적백분비.결과 부S조미견뇌경사발생;여S조비교,HIBI조화Ⅰ조T1-4시수손측해마화피층사망신경원계수승고,VEGF표체상조(P＜0.05);여HIBI비교,Ⅰ조뇌경사체적백분비강저,T1.2시수손측해마화피층사망신경원계수강저,VEGF표체상조(P＜0.05),S조각시점수손측해마화피층사망신경원계수화VEGF표체비교차이무통계학의의(P＞0.05),HIBI조T3시、Ⅰ조T2시VEGF표체수평체고봉(P＜0.05).Ⅰ조수손측뇌조직병이학손상교HIBI조감경.결론 이불미후처리가능통과상조뇌조직VEGF표체,감경신생대서결혈결양성뇌손상.
Objective To investigate the effect of isoflurane postconditioning on the expression of vascular endothelial growth factor (VEGF) in neonatal rats with hypoxic-ischemic brain injury (HIBI).Methods One hundred and fifty-six 7-day-old Sprague-Dawley rats were randomly divided into 3 groups (n =52 each) using a random number table:sham operation group (S group),HIBI group,and isoflurane post-conditioning group (Ⅰ group).Brain ischemia was induced by ligation of the left common carotid artery followed by inhalation of 8％ O2 + 92％ N2 for 2 h at 37 ℃.The rats were exposed to 1％ isoflurane for 1 h (group Ⅰ) or to 30％ oxygen-70％ nitrogen for 1 h (HIBI group) starting from 2 h of hypoxia.The left common carotid artery was only separated and then the rats were exposed to 30％ oxygen and 70％ nitrogen for 1 h in S group.The rats were sacrificed at 1,2,3 and 7 days after HIBI (T1-4),and their brains on the damaged side were harvested for microscopic examination and for determination of the dead neuron counts in the hippocampi and cortex and expression of VEGF (by immunohistochemistry and Western blot).The cerebral infarct size was detected at T2.Results No cerebral infarct was observed in S group.Compared with S group,the cerebral infarct size and counts of dead neurons in the hippocampi and cortex on the damaged side at T1-4 were significantly increased,and the expression of VEGF was up-regulated in H IBI and Ⅰ groups (P ＜ 0.05).Compared with HIBI group,the cerebral infarct size and counts of dead neurons in the hippocampi and cortex on the damaged side at T1,2 were significantly decreased,and the expression of VEGF was up-regulated in Ⅰ group (P ＜ 0.05).There was no significant difference in the counts of dead neurons in the hippocampi and cortex on the damaged side and expression of VEGF between the time points in S group (P ＞ 0.05).The expression of VEGF peaked at T3 in HIBI group and T2 in Ⅰ group (P ＜ 0.05).The pathological changes of brain tissues on the damaged side were significantly attenuated in group Ⅰ as compared with HIBI group.Conclusion Isoflurane postconditioning reduces HIBI in neonatal rats possibility through upregulating the expression of VEGF in brain tissues.