中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
4期
484-487
,共4页
邵建林%万晓红%王雁%梁荣毕%衡新华
邵建林%萬曉紅%王雁%樑榮畢%衡新華
소건림%만효홍%왕안%량영필%형신화
血红素氧化酶(脱环)%麻醉药,吸入%缺血预处理%再灌注损伤%神经元%海马%细胞凋亡
血紅素氧化酶(脫環)%痳醉藥,吸入%缺血預處理%再灌註損傷%神經元%海馬%細胞凋亡
혈홍소양화매(탈배)%마취약,흡입%결혈예처리%재관주손상%신경원%해마%세포조망
Heme oxygenase (decyclizing)%Anesthetics,inhalation%Ischemie preconditioning%Reperfusion injury%Neurons%Hippocampns%Apoptosis
目的 探讨血红素氧合酶-1(HO-1)在七氟烷预处理抑制大鼠氧糖剥夺海马神经元凋亡中的作用.方法 出生48 h内的Wistar大鼠,体外培养海马神经元,随机分为6组,每组108孔,正常对照组(C组):不做任何处理;2%七氟烷预处理组(S1组):2%七氟烷预处理60 min后正常培养24 h;OGD组:缺糖缺氧45 min后复糖复氧,再正常培养24 h以制备氧糖剥夺模型;2%七氟烷预处理+OGD 组(S1+OGD组)和4%七氟烷预处理+OGD组(S2+OGD组):分别经2%、4%七氟烷预处理后制备氧糖剥夺模型;4%七氟烷预处理+ZnPPⅨ+OGD(Z组):4%七氟烷预处理同时在培养液中加入ZnPPⅨ(终浓度10 μmol/L),其余处理同S2+OGD组.正常培养24 h时检测神经元存活率、凋亡率和HO-1蛋白及其mRNA的表达水平.结果 与C组比较,OGD组、S1+OGD组、S2+OGD组和Z组海马神经元存活率降低,凋亡率升高,海马神经元HO-1 mRNA及其蛋白表达上调,S1组海马神经元HO-1 mRNA 及其蛋白表达上调(P<0.01),神经元存活率、凋亡率差异无统计学意义(P>0.05);与OGD组比较,S1+OGD组、S2+OGD组海马神经元存活率升高,凋亡率降低,海马神经元HO-1 mRNA及其蛋白表达上调,Z组上述指标差异无统计学意义(P>0.05);与S1+OGD组比较,S2+OGD组海马神经元存活率升高,凋亡率降低,海马神经元HO-1 mRNA及其蛋白表达上调(P<0.01);与S2+OGD组比较,Z组海马神经元存活率降低,凋亡率升高,海马神经元HO-1 mRNA及其蛋白表达下调(P<0.01).结论 HO-1可能参与了七氟烷预处理抑制大鼠氧糖剥夺海马神经元凋亡的机制.
目的 探討血紅素氧閤酶-1(HO-1)在七氟烷預處理抑製大鼠氧糖剝奪海馬神經元凋亡中的作用.方法 齣生48 h內的Wistar大鼠,體外培養海馬神經元,隨機分為6組,每組108孔,正常對照組(C組):不做任何處理;2%七氟烷預處理組(S1組):2%七氟烷預處理60 min後正常培養24 h;OGD組:缺糖缺氧45 min後複糖複氧,再正常培養24 h以製備氧糖剝奪模型;2%七氟烷預處理+OGD 組(S1+OGD組)和4%七氟烷預處理+OGD組(S2+OGD組):分彆經2%、4%七氟烷預處理後製備氧糖剝奪模型;4%七氟烷預處理+ZnPPⅨ+OGD(Z組):4%七氟烷預處理同時在培養液中加入ZnPPⅨ(終濃度10 μmol/L),其餘處理同S2+OGD組.正常培養24 h時檢測神經元存活率、凋亡率和HO-1蛋白及其mRNA的錶達水平.結果 與C組比較,OGD組、S1+OGD組、S2+OGD組和Z組海馬神經元存活率降低,凋亡率升高,海馬神經元HO-1 mRNA及其蛋白錶達上調,S1組海馬神經元HO-1 mRNA 及其蛋白錶達上調(P<0.01),神經元存活率、凋亡率差異無統計學意義(P>0.05);與OGD組比較,S1+OGD組、S2+OGD組海馬神經元存活率升高,凋亡率降低,海馬神經元HO-1 mRNA及其蛋白錶達上調,Z組上述指標差異無統計學意義(P>0.05);與S1+OGD組比較,S2+OGD組海馬神經元存活率升高,凋亡率降低,海馬神經元HO-1 mRNA及其蛋白錶達上調(P<0.01);與S2+OGD組比較,Z組海馬神經元存活率降低,凋亡率升高,海馬神經元HO-1 mRNA及其蛋白錶達下調(P<0.01).結論 HO-1可能參與瞭七氟烷預處理抑製大鼠氧糖剝奪海馬神經元凋亡的機製.
목적 탐토혈홍소양합매-1(HO-1)재칠불완예처리억제대서양당박탈해마신경원조망중적작용.방법 출생48 h내적Wistar대서,체외배양해마신경원,수궤분위6조,매조108공,정상대조조(C조):불주임하처리;2%칠불완예처리조(S1조):2%칠불완예처리60 min후정상배양24 h;OGD조:결당결양45 min후복당복양,재정상배양24 h이제비양당박탈모형;2%칠불완예처리+OGD 조(S1+OGD조)화4%칠불완예처리+OGD조(S2+OGD조):분별경2%、4%칠불완예처리후제비양당박탈모형;4%칠불완예처리+ZnPPⅨ+OGD(Z조):4%칠불완예처리동시재배양액중가입ZnPPⅨ(종농도10 μmol/L),기여처리동S2+OGD조.정상배양24 h시검측신경원존활솔、조망솔화HO-1단백급기mRNA적표체수평.결과 여C조비교,OGD조、S1+OGD조、S2+OGD조화Z조해마신경원존활솔강저,조망솔승고,해마신경원HO-1 mRNA급기단백표체상조,S1조해마신경원HO-1 mRNA 급기단백표체상조(P<0.01),신경원존활솔、조망솔차이무통계학의의(P>0.05);여OGD조비교,S1+OGD조、S2+OGD조해마신경원존활솔승고,조망솔강저,해마신경원HO-1 mRNA급기단백표체상조,Z조상술지표차이무통계학의의(P>0.05);여S1+OGD조비교,S2+OGD조해마신경원존활솔승고,조망솔강저,해마신경원HO-1 mRNA급기단백표체상조(P<0.01);여S2+OGD조비교,Z조해마신경원존활솔강저,조망솔승고,해마신경원HO-1 mRNA급기단백표체하조(P<0.01).결론 HO-1가능삼여료칠불완예처리억제대서양당박탈해마신경원조망적궤제.
Objective To investigate the role of HO-1 in inhibition of oxygen-glucose deprivation (OGD)-induced apoptosis in rat hippocampal neurons by sevoflurane preconditioning.Methods Hippoeanlpal neurons of newborn Wistar rats (<48 h) were cultured in vitro.Tne neurons were randomly divided into 6 groups with 108 wells in each group:control group(group C),2% sevoflurane preconditioning group (group S1),OGD group,S1 +OGD group,4% sevoflurane preconditioning+OGD group (group S2+OGD),and 4% sevoflurane preconditioning+ZnPPⅨ+OGD group(group Z).Group C received no treatment.The neurons were cultured for 24 h after 2% sevoflurane preconditioning in group S1.For OGD experiments,the neurons were placed in deoxygenated glucose-free medium and sealed under 95% N2-5% CO2 in an anaerobic chamber equilibrated to 37℃ and 100%humidity for 45 min.then OGD was terminated by replacement of the stored medium and returning the cultures to a standard incubator maintained at 37℃ in 5% C02 and the neurons were cultured for 24 h as described by Ray et al. The OGD model was established after 2% and 4% sevoflurane preconditioning in group S1 + OGD and S2 + OGD respectively. In group Z, when the neurons were preconditioned with 4% sevoflurane, ZnPPⅨ was added to the culture medium at the same time, and the other procedures were the same as those in group S2 + OGD. The neuron viability, apoptesis rate, and expression of HO-I protein and mRNA were detected at 24 h of culture. Results Compared with group C, neuron viability was significantly decreased,apoptosis rate was significantly increased, and expression of HO-1 protein and mRNA was up-regulated in group OGD, S1 + OGD, S2 + OGD and Z, expression of HO-1 protein and mRNA was up-regulated in group S1 ( P < 0.01 ), but no significant change was found in neuron viability and apoptosis rate in group S1 ( P > 0.05). Compared with group OGD, neuron viability was significantly increased, apoptosis rate was significantly decreased, and expression of HO-1 protein and mRNA was up-regulated in group S1 + OGD and S2 + OGD ( P < 0.01), but no significant change was found in the indexes mentioned above in group Z ( P > 0.05 ). Neuron viability was significantly higher, apoptosis rate lower and expression of HO-1 protein and mRNA higher in group S2 + OGD than in group S1 + OGD ( P < 0.01). Neuron viability was significantly lower, apoptosis rate higher and expression of HO-1 protein and mRNA lower in group Z than in group S2+OGD(P<0.01).Conclusion HO-1 is involved in the inhibition of OGD-indueed apoptosis in rat hippocampal neurons by sevoflurane preconditioning.
