国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
International Journal of Anesthesiology and Resuscitation
2015年
9期
780-784
,共5页
右美托咪定%七氟醚%认知功能障碍%海马%凋亡
右美託咪定%七氟醚%認知功能障礙%海馬%凋亡
우미탁미정%칠불미%인지공능장애%해마%조망
Dexmedetomidine%Sevoflurane%Cognitive dysfunction%Hippocampus%Apoptosis
目的 探讨腹腔注射右美托咪定(dexmedetomidine,Dex)能否减轻七氟醚诱导的新生大鼠海马细胞凋亡和远期认知功能障碍. 方法 48只出生7d的Sprague-Dawley(SD)大鼠采用随机数字表法分为4组(每组12只):对照组(C组)、25 μg/kg Dex单纯腹腔注射组(D组)、3％七氟醚吸入组(S组)和25 μg/kg Dex干预组(DS组),每组实验连续重复3d.吸入处理后每组又采用随机数字表法分为2个亚组(A组和B组,每组6只),A组2h后用Western blot法检测组织内海马激活型Caspase-3,脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(terminal-deoxynucleotidyl transferase mediated nick end labeling,TUNEL)检测海马CA1区细胞凋亡;B组继续饲养到3周后采用Morrs水迷宫实验评估大鼠的学习和记忆功能. 结果 S组和DS组新生大鼠CA1区TUNEL阳性细胞[(45±5),(33±6)个/mm2]高于C组[(18±4)个/mm2](P＜0.05);S组和DS组新生大鼠CA1区激活型Caspase-3表达[(1.40±0.25),(1.22±0.15)]高于对照组(0.30±0.20) (P＜0.05);与S组比较,DS组新生大鼠的CA1区TUNEL阳性细胞和激活型Caspase-3表达减少(P＜0.05).与C组比较,S组和DS组新生大鼠远期的认知和学习能力下降;与S组比较,DS组新生大鼠远期的认知和学习能力增强. 结论 多次吸入3％的七氟醚能诱导新生大鼠海马细胞凋亡和认知功能障碍,而预先腹腔注射25 μg/kg Dex能减轻七氟醚诱导的海马细胞凋亡和远期认识功能障碍.
目的 探討腹腔註射右美託咪定(dexmedetomidine,Dex)能否減輕七氟醚誘導的新生大鼠海馬細胞凋亡和遠期認知功能障礙. 方法 48隻齣生7d的Sprague-Dawley(SD)大鼠採用隨機數字錶法分為4組(每組12隻):對照組(C組)、25 μg/kg Dex單純腹腔註射組(D組)、3％七氟醚吸入組(S組)和25 μg/kg Dex榦預組(DS組),每組實驗連續重複3d.吸入處理後每組又採用隨機數字錶法分為2箇亞組(A組和B組,每組6隻),A組2h後用Western blot法檢測組織內海馬激活型Caspase-3,脫氧覈糖覈苷痠末耑轉移酶介導的缺口末耑標記法(terminal-deoxynucleotidyl transferase mediated nick end labeling,TUNEL)檢測海馬CA1區細胞凋亡;B組繼續飼養到3週後採用Morrs水迷宮實驗評估大鼠的學習和記憶功能. 結果 S組和DS組新生大鼠CA1區TUNEL暘性細胞[(45±5),(33±6)箇/mm2]高于C組[(18±4)箇/mm2](P＜0.05);S組和DS組新生大鼠CA1區激活型Caspase-3錶達[(1.40±0.25),(1.22±0.15)]高于對照組(0.30±0.20) (P＜0.05);與S組比較,DS組新生大鼠的CA1區TUNEL暘性細胞和激活型Caspase-3錶達減少(P＜0.05).與C組比較,S組和DS組新生大鼠遠期的認知和學習能力下降;與S組比較,DS組新生大鼠遠期的認知和學習能力增彊. 結論 多次吸入3％的七氟醚能誘導新生大鼠海馬細胞凋亡和認知功能障礙,而預先腹腔註射25 μg/kg Dex能減輕七氟醚誘導的海馬細胞凋亡和遠期認識功能障礙.
목적 탐토복강주사우미탁미정(dexmedetomidine,Dex)능부감경칠불미유도적신생대서해마세포조망화원기인지공능장애. 방법 48지출생7d적Sprague-Dawley(SD)대서채용수궤수자표법분위4조(매조12지):대조조(C조)、25 μg/kg Dex단순복강주사조(D조)、3％칠불미흡입조(S조)화25 μg/kg Dex간예조(DS조),매조실험련속중복3d.흡입처리후매조우채용수궤수자표법분위2개아조(A조화B조,매조6지),A조2h후용Western blot법검측조직내해마격활형Caspase-3,탈양핵당핵감산말단전이매개도적결구말단표기법(terminal-deoxynucleotidyl transferase mediated nick end labeling,TUNEL)검측해마CA1구세포조망;B조계속사양도3주후채용Morrs수미궁실험평고대서적학습화기억공능. 결과 S조화DS조신생대서CA1구TUNEL양성세포[(45±5),(33±6)개/mm2]고우C조[(18±4)개/mm2](P＜0.05);S조화DS조신생대서CA1구격활형Caspase-3표체[(1.40±0.25),(1.22±0.15)]고우대조조(0.30±0.20) (P＜0.05);여S조비교,DS조신생대서적CA1구TUNEL양성세포화격활형Caspase-3표체감소(P＜0.05).여C조비교,S조화DS조신생대서원기적인지화학습능력하강;여S조비교,DS조신생대서원기적인지화학습능력증강. 결론 다차흡입3％적칠불미능유도신생대서해마세포조망화인지공능장애,이예선복강주사25 μg/kg Dex능감경칠불미유도적해마세포조망화원기인식공능장애.
Objective To investigate whether dexmedetomidine(Dex) could alleviate the apoptosis of hippocampus cell and long-time cognitive dysfunction induced by sevoflurane (Sev) in neonatal rats.Methods Forty-eight Sprague-Dawley (SD) rats in postnatal 7 d were randomly assigned into 4 groups (n=12):control group (group C),25 μg/kg Dex intraperitoneal injection group (group D),3％ Sev inhaling group (group S) and 25 μg/kg Dex intervention group (group DS).Each group was randomly divided into 2 subgroups (subgroup A and subgroup B,6 rats in every subgroup).Twenty-four hours after completion of Sev exposure in subgroup A,the activation of caspase-3 in hippocampus were analyzed by Western blot,and the neuronal apoptosis in the CA1 region of the hippocampus were detected by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) method.The rats' cognitive function was evaluated using Morris maze experiment in subgroup B.Results Compared with group C,the expression of TUNEL positive cells in group S and group DS increased[(45±5)/mm2 vs (18±4)/mm2 and (33±6)/mm2 vs (18±4)/mm2,respectively](P＜0.05).Compared with group C,the expression of cleaved Caspase-3 in group S and group DS increased[(1.40±0.25) vs (0.30±0.20)and (1.22±0.15) vs (0.30±0.20),respectively](P＜0.05).The expression of TUNEL positive cells and cleaved Caspase-3 decreased in group DS compared with group S (P＜0.05).Compared with group C.The cognitive function of rats declined in the group S and group DS.Compared with group S,the cognitive dysfunction of rats alleviated in group DS.Conclusions Repeatedly inhaling 3％Sev can induce the apoptosis of hippocampus cells and long-time cognitive dysfunction.25 μg/kg Dex intraperitoneal injection before inhaling Sev can alleviate the neurotoxicity induced by Sev.
