国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2009年
16期
961-965
,共5页
徐琳%雷法特·别克强塔伊夫%李秀娟%王娜%克拉拉·阿巴斯
徐琳%雷法特·彆剋彊塔伊伕%李秀娟%王娜%剋拉拉·阿巴斯
서림%뢰법특·별극강탑이부%리수연%왕나%극랍랍·아파사
Gq/11蛋白%急性肺损伤%脑%大鼠
Gq/11蛋白%急性肺損傷%腦%大鼠
Gq/11단백%급성폐손상%뇌%대서
Gq/11 protein%Acute lung injury%Brain%Rat
目的 观察急性肺损伤(acute lung injury,ALI)大鼠脑组织中Gq/11蛋白的动态改变,从分子水平研究油酸(OA)性ALI导致脑损伤以及ALI导致多器官功能障碍综合征的可能机制,为ALI和多器官功能障碍综合征的发病机制提供实验和理论依据.方法 用尾静脉注射OA法复制ALI大鼠模型,将40只健康雄性Wistar大鼠随机分为对照组(C组)和实验组(OA组),OA组又根据不同时限将其分为30 min、60 min、90 min和120 min 4个亚组.观察检测各组大鼠血气(pH、PaO2、PaCO2)、平均动脉压(MABP)、血浆及脑组织乳酸脱氢酶(LDH)、肌酸激酶(CK)、丙二醛(MDA).免疫印迹法检测各组大鼠脑组织中的Gq/11蛋白含量.结果 Gq/11蛋白含量:除OA30 min组外,其余OA各组随着时间延长较C组分别增加至(141.85±33.82)%、(165.84±30.27)%、(174.31±32.52)%(P<0.01).除OA 30 min组外,其余OA各组血浆MDA含量均较c组升高(P<0.01);OA 30 min组和OA 60 min组脑组织MDA含量与C组比较差异无统计学意义,OA 90 min组和OA 120 min组脑组织MDA含量较C组升高(P<0.01).OA各组血浆LDH活性均较C组升高(P<0.01);除OA 30 min组外,其余OA各组脑组织LDH活性均较C组升高(P<0.01).脑组织CK活性在60 min时达到峰值(P<0.01),以后呈下降趋势.结论 ALI可导致远隔器官脑的损伤,引起细胞信号转导功能异常和脑代谢及形态的变化,Gq/11蛋白的高表达变化可能参与了ALl过程及脑损害的病理性信号转导.
目的 觀察急性肺損傷(acute lung injury,ALI)大鼠腦組織中Gq/11蛋白的動態改變,從分子水平研究油痠(OA)性ALI導緻腦損傷以及ALI導緻多器官功能障礙綜閤徵的可能機製,為ALI和多器官功能障礙綜閤徵的髮病機製提供實驗和理論依據.方法 用尾靜脈註射OA法複製ALI大鼠模型,將40隻健康雄性Wistar大鼠隨機分為對照組(C組)和實驗組(OA組),OA組又根據不同時限將其分為30 min、60 min、90 min和120 min 4箇亞組.觀察檢測各組大鼠血氣(pH、PaO2、PaCO2)、平均動脈壓(MABP)、血漿及腦組織乳痠脫氫酶(LDH)、肌痠激酶(CK)、丙二醛(MDA).免疫印跡法檢測各組大鼠腦組織中的Gq/11蛋白含量.結果 Gq/11蛋白含量:除OA30 min組外,其餘OA各組隨著時間延長較C組分彆增加至(141.85±33.82)%、(165.84±30.27)%、(174.31±32.52)%(P<0.01).除OA 30 min組外,其餘OA各組血漿MDA含量均較c組升高(P<0.01);OA 30 min組和OA 60 min組腦組織MDA含量與C組比較差異無統計學意義,OA 90 min組和OA 120 min組腦組織MDA含量較C組升高(P<0.01).OA各組血漿LDH活性均較C組升高(P<0.01);除OA 30 min組外,其餘OA各組腦組織LDH活性均較C組升高(P<0.01).腦組織CK活性在60 min時達到峰值(P<0.01),以後呈下降趨勢.結論 ALI可導緻遠隔器官腦的損傷,引起細胞信號轉導功能異常和腦代謝及形態的變化,Gq/11蛋白的高錶達變化可能參與瞭ALl過程及腦損害的病理性信號轉導.
목적 관찰급성폐손상(acute lung injury,ALI)대서뇌조직중Gq/11단백적동태개변,종분자수평연구유산(OA)성ALI도치뇌손상이급ALI도치다기관공능장애종합정적가능궤제,위ALI화다기관공능장애종합정적발병궤제제공실험화이론의거.방법 용미정맥주사OA법복제ALI대서모형,장40지건강웅성Wistar대서수궤분위대조조(C조)화실험조(OA조),OA조우근거불동시한장기분위30 min、60 min、90 min화120 min 4개아조.관찰검측각조대서혈기(pH、PaO2、PaCO2)、평균동맥압(MABP)、혈장급뇌조직유산탈경매(LDH)、기산격매(CK)、병이철(MDA).면역인적법검측각조대서뇌조직중적Gq/11단백함량.결과 Gq/11단백함량:제OA30 min조외,기여OA각조수착시간연장교C조분별증가지(141.85±33.82)%、(165.84±30.27)%、(174.31±32.52)%(P<0.01).제OA 30 min조외,기여OA각조혈장MDA함량균교c조승고(P<0.01);OA 30 min조화OA 60 min조뇌조직MDA함량여C조비교차이무통계학의의,OA 90 min조화OA 120 min조뇌조직MDA함량교C조승고(P<0.01).OA각조혈장LDH활성균교C조승고(P<0.01);제OA 30 min조외,기여OA각조뇌조직LDH활성균교C조승고(P<0.01).뇌조직CK활성재60 min시체도봉치(P<0.01),이후정하강추세.결론 ALI가도치원격기관뇌적손상,인기세포신호전도공능이상화뇌대사급형태적변화,Gq/11단백적고표체변화가능삼여료ALl과정급뇌손해적병이성신호전도.
Objective To observe the change of Gq/11 protein concentration in the brain of rats during acute lung injury(ALI) and explore the pathophysiological mechanism of multiple organ dysfunction syndrome caused by ALI in terms of signal conduction. Methods ALl rat model was reproduced by intravenous injection of oleic acid (OA). Forty male Wistar rats were randomly divided into control group(C group) and experiment group(OA group). OA group included four subsections: OA30, 60, 90,120 min group. Blood gas indexes (pH, PaO2, PaCO2), mean arterial blood pressure and lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA) of plasma and brain were measured. Gq/11 protein concentration was examined by Western blot. Results Gq/11 protein concentration in the brain of OA groups (except OA 30 min group) respectively increased to ( 141.85 ± 33.82 )%, ( 165.84 ± 30.27) %,(174.31±4-32.52)% ( P <0.01). MDA content in the plasma of OA groups (except OA 30 min group) was higher than that of C group( P <0.01). MDA content in the brain of OA 90 min group and OA 120 min group was higher than that of C group( P<0.01). LDH activity in the plasma of OA groups was higher than that of C group( P <0.01). LDH activity in the brain of OA groups (except OA 30 min group) was higher than that of C group(P<0.01). CK activity in the brain reached peak at OA60 min group( P<0.01) and then decreased. Conclusions Upregulation of Gq/11 protein concentration in the brain may play a role in ALl.
