CAJ | 학술논문

目的探讨右美托咪定对创伤性脑损伤大鼠海马神经元自噬的影响.方法健康雄性SD大鼠240只,12～ 16周龄,体重340～ 370 g,采用随机数字表法分为3组(n=80):假手术组(S组)、创伤性脑损伤组(TBI组)和右美托咪定组(Dex组).采用改良自由落体装置制备创伤性脑损伤模型.Dex组于模型制备后即刻腹腔注射右美托咪定15 μg/kg.于模型制备后24和48 h时进行神经功能缺陷(NDS)评分和Morris水迷宫实验;取脑组织,测定脑水含量.于模型制备后6、12、24和48 h时,采用Western blot法测定海马LC3Ⅱ的表达水平.结果与S组比较,TBI组模型制备后24和48 h时脑水含量和NDS评分升高,逃避潜伏期延长,模型制备后6、12、24和48 h时海马LC3Ⅱ表达上调(P＜0.05);与TBI组比较,Dex组模型制备后24和48 h时脑水含量和NDS评分降低,模型制备后48 h时逃避潜伏期缩短,模型制备后6、12、24 h和48时海马LC3Ⅱ表达下调(P＜0.05).结论右美托咪定减轻大鼠创伤性脑损伤的机制可能与抑制海马神经元自噬有关.
목적 탐토우미탁미정대창상성뇌손상대서해마신경원자서적영향.방법 건강웅성SD대서240지,12～ 16주령,체중340～ 370 g,채용수궤수자표법분위3조(n=80):가수술조(S조)、창상성뇌손상조(TBI조)화우미탁미정조(Dex조).채용개량자유락체장치제비창상성뇌손상모형.Dex조우모형제비후즉각복강주사우미탁미정15 μg/kg.우모형제비후24화48 h시진행신경공능결함(NDS)평분화Morris수미궁실험;취뇌조직,측정뇌수함량.우모형제비후6、12、24화48 h시,채용Western blot법측정해마LC3Ⅱ적표체수평.결과 여S조비교,TBI조모형제비후24화48 h시뇌수함량화NDS평분승고,도피잠복기연장,모형제비후6、12、24화48 h시해마LC3Ⅱ표체상조(P＜0.05);여TBI조비교,Dex조모형제비후24화48 h시뇌수함량화NDS평분강저,모형제비후48 h시도피잠복기축단,모형제비후6、12、24 h화48시해마LC3Ⅱ표체하조(P＜0.05).결론 우미탁미정감경대서창상성뇌손상적궤제가능여억제해마신경원자서유관.
Objective To evaluate the effect of dexmedetomidine on autophagy in the hippocampal neurons of rats with traumatic brain injury (TBI).Methods Adult male Sprague-Dawley rats,aged 12-16 weeks,weighing 340-370 g,were randomly divided into 3 groups (n=80 each) using a random number table:sham operation group (group S),traumatic brain injury group (group TBI) and dexmedetomidine group (group Dex).The rats were subjected to a diffuse cortical impact injury caused by a modified weight-drop device to induce TBI.Dexmedetomidine 15 μg/kg was injected intravenously immediately after TBI in Dex group.At 24 and 48 h after TBI,neurological deficit score (NDS) was assessed,Morris water maze test was performed,and brains were removed for detection of brain water content in the brain tissue.At 6,12,24 and 48 h after TBI,the expression of hippocampal LC3]Ⅱ was determined using Western blot analysis.Results Compared with group S,brain water content and NDS were significantly increased at 24 and 48 h after TBI,the escape latency was prolonged,and the expression of hippocampal LC3 Ⅱ was upregulated at 6,12,24 and 48 h after TBI in TBI group.Compared with TBI group,brain water content and NDS were significantly decreased at 24 and 48 h after TBI,the escape latency was shortened,and the expression of hippocampal LC3 Ⅱ was down-regulated at 6,12,24 and 48 h after TBI in Dex group.Conclusion The mechanism by which dexmedetomidine reduces TBI is related to inhibition of autophagy in the hippocampal neurons of rats.