中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
3期
276-279
,共4页
李捷萌%陈彦青%刘荣国%吴晓丹
李捷萌%陳彥青%劉榮國%吳曉丹
리첩맹%진언청%류영국%오효단
1-磷脂酰肌醇3-激酶%蛋白激酶类%二氮嗪%缺血预处理%细胞低氧%氧%海马%神经元
1-燐脂酰肌醇3-激酶%蛋白激酶類%二氮嗪%缺血預處理%細胞低氧%氧%海馬%神經元
1-린지선기순3-격매%단백격매류%이담진%결혈예처리%세포저양%양%해마%신경원
1-Phesphatidylinositol 3-kirmse%Protein kinases%Diazoxide%lschemic preconditioning%Cell hypoxia%Oxygen%Hippocampus%Neurons
目的 探讨PDK/Akt信号转导通路在二氮嗪预处理减轻大鼠海马缺氧复氧损伤中的作用.方法 新生SD大鼠,出生时间<24 h,体重5-6 g,断头取海马组织,胰蛋白酶消化后,将神经元接种于96孔板或直径35 mm培养皿中,培养12 d后,随机分为6组:对照组(C组)、缺氧复氧组(HR组)、二氮嗪100μmol/L预处理组(Dz组)、二氮嗪100 μmol/L预处理+5-羟癸酸100μmol/L预处理组(DZ+HD组)、5-羟癸酸100 μmol/L预处理组(HD组)和二氮嗪100 μmol/L预处理+LY294002 50μmol/L预处理组(Dz+LY组),每组48孔或12皿.C组不给予任何处理,其余5组每天给予相应药物预处理l h,连续3 d,然后缺氧4 h,复氧24 h,测定神经元活力、凋亡率、Akt、Bcl-2和Bax的表达水平.结果 与C组比较,其余各组海马神经元活力降低.凋亡率升高,Akt和Bcl-2和Bax表达上调(P<0.01);与HR组比较.DZ组海马神经元活力升高.凋亡率降低,Altt和Bel-2表达上调,Bax表达下调(P<0.01);与Dz组比较,DZ+HD组、HD组和Dz+LY组海马神经元活力降低,凋亡率升高.Akt和Bel-2表达下调,Bax表达上调(P<0.01).结论 二氮嗪预处理可能通过激活PDK/Akt信号转导通路,上调Bel-2表达,下调Bax表达,抑制神经元凋亡,从而减轻大鼠海马缺氧复氧损伤.
目的 探討PDK/Akt信號轉導通路在二氮嗪預處理減輕大鼠海馬缺氧複氧損傷中的作用.方法 新生SD大鼠,齣生時間<24 h,體重5-6 g,斷頭取海馬組織,胰蛋白酶消化後,將神經元接種于96孔闆或直徑35 mm培養皿中,培養12 d後,隨機分為6組:對照組(C組)、缺氧複氧組(HR組)、二氮嗪100μmol/L預處理組(Dz組)、二氮嗪100 μmol/L預處理+5-羥癸痠100μmol/L預處理組(DZ+HD組)、5-羥癸痠100 μmol/L預處理組(HD組)和二氮嗪100 μmol/L預處理+LY294002 50μmol/L預處理組(Dz+LY組),每組48孔或12皿.C組不給予任何處理,其餘5組每天給予相應藥物預處理l h,連續3 d,然後缺氧4 h,複氧24 h,測定神經元活力、凋亡率、Akt、Bcl-2和Bax的錶達水平.結果 與C組比較,其餘各組海馬神經元活力降低.凋亡率升高,Akt和Bcl-2和Bax錶達上調(P<0.01);與HR組比較.DZ組海馬神經元活力升高.凋亡率降低,Altt和Bel-2錶達上調,Bax錶達下調(P<0.01);與Dz組比較,DZ+HD組、HD組和Dz+LY組海馬神經元活力降低,凋亡率升高.Akt和Bel-2錶達下調,Bax錶達上調(P<0.01).結論 二氮嗪預處理可能通過激活PDK/Akt信號轉導通路,上調Bel-2錶達,下調Bax錶達,抑製神經元凋亡,從而減輕大鼠海馬缺氧複氧損傷.
목적 탐토PDK/Akt신호전도통로재이담진예처리감경대서해마결양복양손상중적작용.방법 신생SD대서,출생시간<24 h,체중5-6 g,단두취해마조직,이단백매소화후,장신경원접충우96공판혹직경35 mm배양명중,배양12 d후,수궤분위6조:대조조(C조)、결양복양조(HR조)、이담진100μmol/L예처리조(Dz조)、이담진100 μmol/L예처리+5-간계산100μmol/L예처리조(DZ+HD조)、5-간계산100 μmol/L예처리조(HD조)화이담진100 μmol/L예처리+LY294002 50μmol/L예처리조(Dz+LY조),매조48공혹12명.C조불급여임하처리,기여5조매천급여상응약물예처리l h,련속3 d,연후결양4 h,복양24 h,측정신경원활력、조망솔、Akt、Bcl-2화Bax적표체수평.결과 여C조비교,기여각조해마신경원활력강저.조망솔승고,Akt화Bcl-2화Bax표체상조(P<0.01);여HR조비교.DZ조해마신경원활력승고.조망솔강저,Altt화Bel-2표체상조,Bax표체하조(P<0.01);여Dz조비교,DZ+HD조、HD조화Dz+LY조해마신경원활력강저,조망솔승고.Akt화Bel-2표체하조,Bax표체상조(P<0.01).결론 이담진예처리가능통과격활PDK/Akt신호전도통로,상조Bel-2표체,하조Bax표체,억제신경원조망,종이감경대서해마결양복양손상.
Objective To investigate the role of PDK/Akt signal transduetion pathway in the protection of rat hippocampal neulons by diazoxide preconditioning against anoxia-reoxygenation injury.Methods Newborn SD rats(<24 h after birth)weighing 5-6 g were decapitated and hippocampal tissue was isolated and hippcamapal neuronfl were prepared by digestion with trypsin.After being cultured for 12 days,the hippocampal neurons were randomly divided into 6 groups:group Ⅰ control(C),group Ⅱ anoxia-reoxygenation(HR),group Ⅲ diazoxide 100/μmol/L precondidoning+ HR(DZ+HR),group Ⅳ diazoxide 100μmol/L+5-hydroxydecanoate 100 tanol/L preconditioning+HR(DZ+HD+HR),group Ⅴ 5-hydmxydecanoate 100 μmol/L preconditioning +HR(HD+HR)and group Ⅵ diazoxide 100 μmol/L+LY294002 50 μmol/L preconditioning+HR(DZ+LY+HR).The hippoeampal neurons were treated with diazoxide or 5-hydroxydecanoate 1 h per day for 3 days before being subjected to 4 h oxygen deprivation followed by 24 h reoxygermtioa.The neuronsd vitality,apoptosis rate and the expression of Akt.Bcl-2 and Bax were determined.Results Compared with group C.the nelwona]vitality Was signifleandy decreased,the apoptosis rate Was significanfly increased,and the expression of Akt,Bcl-2 and Bax were signiticandy up-regulated in the other 5 group.Compared with group HR.the neuronal vitality was significantly increased.the apoptosis rale was significantly decreased,and the expression of Akt and Bcl-2 were significantly down-regulated while Bax wag sighifieantly up-regulated in group DZ+HR.Compared with group DZ+HR,the neuronal vitality WM signitlcanfly decreased,the apoptosis rate Wills significantly increased,the expression of Akt and Bcl-2 were significantly down-regulated while Bax was significantly up-regulated in group DZ + HD + HR, HD + HR and DZ + LY + HR. Conclusion Diamxide preconditioning may inhibit neuronal apoptosis through activating PI3K/Akt signal traneduction pathway, up-regulating Bcl-2 expression and downregulating Bax expression, and attenuates anoxia-reoxygenation injury in rat hippocampal neurons.
