目的 探讨急性呼吸窘迫综合征(ARDS)大鼠肺、脑、心、肾、肝、小肠中Gq/11蛋白表达及作用.方法 40只Wistar大鼠按随机数字表法分为5组,每组8只.由大鼠尾静脉注射油酸(OA)0.2 ml/kg复制ARDS模型,对照组从尾静脉注射等量生理盐水.模型组分别于制模后30、60、90和120 min检测血浆和各器官中乳酸脱氢酶(LDH)、丙二醛(MDA)、血管紧张素转换酶(ACE);蛋白质免疫印迹法(Western blotting)检测各器官中Gq/11蛋白α活性亚基Gαq/11蛋白表达.结果 与对照组相比,LDH活性于30 min后在血浆和心呈进行性升高[血浆(kU/L):9.69±1.66比6.27±1.70,心(kU/g):0.81±0.12比0.59±0.09],60 min后在肺、脑、肾、小肠呈进行性升高[肺(kU/g):1.15±0.19比0.87±0.11,脑(kU/g):2.27±0.37比1.53±0.61,肾(kU/g):1.13±0.26比0.64±0.09,小肠(kU/g):0.72±0.10比0.60±0.13],90 min后在肝(kU/g)呈进行性升高(0.50±0.14比0.39±0.05,P<0.05或P<0.01);MDA含量于30 min后在心(μmol/g)呈进行性升高(2.20±0.47比1.45±0.27),60 min后在血浆、肺、肾呈进行性升高[血浆(μmol/L):3.10±0.58比2.33±0.35,肺(μmol/g):5.56±1.30比2.05±0.52,肾(μmol/g):1.61±0.27比0.98±0.42],90 min后在脑、肝、小肠呈进行性升高[脑(μmol/g):6.78±1.38比5.83±1.58,肝(μmol/g):2.58±0.68比2.11±0.42,小肠(μmol/g):2.14±0.51比0.81±0.26,P<0.05或P<0.01];ACE活性于60 min后在血浆和肺呈进行性降低[血浆(μmol·min-1·L-1):15.47±1.68比19.87±3.11,肺(μmol·min-1·g-1):20.61±1.81比26.26±1.93],在肾(μmol·min-1·g-1)呈进行性升高(15.92±1.20比13.67±2.26),90 min后在小肠(μmol·min-1·g-1)呈进行性升高(4.42±0.34比3.29±0.24,均P<0.01);Gαq/11蛋白表达于30 min后在肺、小肠呈进行性升高[肺:(119.24±2.38)%比(100.00±18.74)%,小肠:(138.91±23.03)%比(100.00±19.43)%],60 min后在脑、心、肾呈进行性升高[脑:(141.85±33.82)%比(100.00±16.81)%,心:(124.72±24.05)%比(100.00±16.04)%,肾:(123.98±25.74)%比(100.00±8.50)%],90 min后在肝呈进行性升高[(134.34±19.14)%比(100.00±13.04)%,P<0.05或P<0.01].Gαq/11蛋白表达与各器官中LDH的变化呈正相关(r=0.584,P<0.05).结论 ARDS过程中肺、脑、心、肾、肝、小肠中Gq/11蛋白表达有不同程度上调,引发肌醇磷脂信号转导通路活性异常,参与了各器官的损伤发生.
目的 探討急性呼吸窘迫綜閤徵(ARDS)大鼠肺、腦、心、腎、肝、小腸中Gq/11蛋白錶達及作用.方法 40隻Wistar大鼠按隨機數字錶法分為5組,每組8隻.由大鼠尾靜脈註射油痠(OA)0.2 ml/kg複製ARDS模型,對照組從尾靜脈註射等量生理鹽水.模型組分彆于製模後30、60、90和120 min檢測血漿和各器官中乳痠脫氫酶(LDH)、丙二醛(MDA)、血管緊張素轉換酶(ACE);蛋白質免疫印跡法(Western blotting)檢測各器官中Gq/11蛋白α活性亞基Gαq/11蛋白錶達.結果 與對照組相比,LDH活性于30 min後在血漿和心呈進行性升高[血漿(kU/L):9.69±1.66比6.27±1.70,心(kU/g):0.81±0.12比0.59±0.09],60 min後在肺、腦、腎、小腸呈進行性升高[肺(kU/g):1.15±0.19比0.87±0.11,腦(kU/g):2.27±0.37比1.53±0.61,腎(kU/g):1.13±0.26比0.64±0.09,小腸(kU/g):0.72±0.10比0.60±0.13],90 min後在肝(kU/g)呈進行性升高(0.50±0.14比0.39±0.05,P<0.05或P<0.01);MDA含量于30 min後在心(μmol/g)呈進行性升高(2.20±0.47比1.45±0.27),60 min後在血漿、肺、腎呈進行性升高[血漿(μmol/L):3.10±0.58比2.33±0.35,肺(μmol/g):5.56±1.30比2.05±0.52,腎(μmol/g):1.61±0.27比0.98±0.42],90 min後在腦、肝、小腸呈進行性升高[腦(μmol/g):6.78±1.38比5.83±1.58,肝(μmol/g):2.58±0.68比2.11±0.42,小腸(μmol/g):2.14±0.51比0.81±0.26,P<0.05或P<0.01];ACE活性于60 min後在血漿和肺呈進行性降低[血漿(μmol·min-1·L-1):15.47±1.68比19.87±3.11,肺(μmol·min-1·g-1):20.61±1.81比26.26±1.93],在腎(μmol·min-1·g-1)呈進行性升高(15.92±1.20比13.67±2.26),90 min後在小腸(μmol·min-1·g-1)呈進行性升高(4.42±0.34比3.29±0.24,均P<0.01);Gαq/11蛋白錶達于30 min後在肺、小腸呈進行性升高[肺:(119.24±2.38)%比(100.00±18.74)%,小腸:(138.91±23.03)%比(100.00±19.43)%],60 min後在腦、心、腎呈進行性升高[腦:(141.85±33.82)%比(100.00±16.81)%,心:(124.72±24.05)%比(100.00±16.04)%,腎:(123.98±25.74)%比(100.00±8.50)%],90 min後在肝呈進行性升高[(134.34±19.14)%比(100.00±13.04)%,P<0.05或P<0.01].Gαq/11蛋白錶達與各器官中LDH的變化呈正相關(r=0.584,P<0.05).結論 ARDS過程中肺、腦、心、腎、肝、小腸中Gq/11蛋白錶達有不同程度上調,引髮肌醇燐脂信號轉導通路活性異常,參與瞭各器官的損傷髮生.
목적 탐토급성호흡군박종합정(ARDS)대서폐、뇌、심、신、간、소장중Gq/11단백표체급작용.방법 40지Wistar대서안수궤수자표법분위5조,매조8지.유대서미정맥주사유산(OA)0.2 ml/kg복제ARDS모형,대조조종미정맥주사등량생리염수.모형조분별우제모후30、60、90화120 min검측혈장화각기관중유산탈경매(LDH)、병이철(MDA)、혈관긴장소전환매(ACE);단백질면역인적법(Western blotting)검측각기관중Gq/11단백α활성아기Gαq/11단백표체.결과 여대조조상비,LDH활성우30 min후재혈장화심정진행성승고[혈장(kU/L):9.69±1.66비6.27±1.70,심(kU/g):0.81±0.12비0.59±0.09],60 min후재폐、뇌、신、소장정진행성승고[폐(kU/g):1.15±0.19비0.87±0.11,뇌(kU/g):2.27±0.37비1.53±0.61,신(kU/g):1.13±0.26비0.64±0.09,소장(kU/g):0.72±0.10비0.60±0.13],90 min후재간(kU/g)정진행성승고(0.50±0.14비0.39±0.05,P<0.05혹P<0.01);MDA함량우30 min후재심(μmol/g)정진행성승고(2.20±0.47비1.45±0.27),60 min후재혈장、폐、신정진행성승고[혈장(μmol/L):3.10±0.58비2.33±0.35,폐(μmol/g):5.56±1.30비2.05±0.52,신(μmol/g):1.61±0.27비0.98±0.42],90 min후재뇌、간、소장정진행성승고[뇌(μmol/g):6.78±1.38비5.83±1.58,간(μmol/g):2.58±0.68비2.11±0.42,소장(μmol/g):2.14±0.51비0.81±0.26,P<0.05혹P<0.01];ACE활성우60 min후재혈장화폐정진행성강저[혈장(μmol·min-1·L-1):15.47±1.68비19.87±3.11,폐(μmol·min-1·g-1):20.61±1.81비26.26±1.93],재신(μmol·min-1·g-1)정진행성승고(15.92±1.20비13.67±2.26),90 min후재소장(μmol·min-1·g-1)정진행성승고(4.42±0.34비3.29±0.24,균P<0.01);Gαq/11단백표체우30 min후재폐、소장정진행성승고[폐:(119.24±2.38)%비(100.00±18.74)%,소장:(138.91±23.03)%비(100.00±19.43)%],60 min후재뇌、심、신정진행성승고[뇌:(141.85±33.82)%비(100.00±16.81)%,심:(124.72±24.05)%비(100.00±16.04)%,신:(123.98±25.74)%비(100.00±8.50)%],90 min후재간정진행성승고[(134.34±19.14)%비(100.00±13.04)%,P<0.05혹P<0.01].Gαq/11단백표체여각기관중LDH적변화정정상관(r=0.584,P<0.05).결론 ARDS과정중폐、뇌、심、신、간、소장중Gq/11단백표체유불동정도상조,인발기순린지신호전도통로활성이상,삼여료각기관적손상발생.
Objective To observe the dynamic alteration in Gq/11 protein expression in the lung, brain, heart, kidney, liver and small intestine of rats suffering from acute respiratory distress syndrome (ARDS), and to explore the pathophysiological mechanism of ARDS in terms of signal transduction. Methods Forty male Wistar rats were randomly divided into oleic acid (OA) groups (n=32) and control group (n=8). OA groups included four subgroups: 30, 60, 90, 120 minutes (each n=8). An ARDS model in rats was reproduced by intravenous injection of OA 0.2 ml/kg in 2 minutes, and control group was given normal saline by the same way. Lactate dehydrogenase (LDH), malondialdehyde (MDA) and angiotensin converting enzyme (ACE) in the plasma and the above-mentioned organs were measured. Gαq/11 protein expression in these organs was examined by Western blotting. Results Compared with control group, LDH activity in the plasma and the heart 30 minutes after injection of OA gradually increased (plasma (kU/L): 9.69±1.66 vs. 6.27±1.70, heart (kU/g): 0.81±0.12 vs. 0.59±0.09), and in the lung, brain, kidney, and small intestine 60 minutes after injection of OA also gradually increased (lung (kU/g): 1.15±0.19 vs. 0.87±0.11, brain (kU/g): 2.27±0.37 vs. 1.53±0.61, kidney (kU/g): 1.13±0.26 vs. 0.64±0.09, small intestine (kU/g): 0.72±0.10 vs. 0.60±0.13), and in the liver (kU/g) 90 minutes after injection of OA gradually increased (0.50±0.14 vs. 0.39±0.05, P<0.05 or P<0.0１). MDA concentration in the heart (μmol/g) 30 minutes after injection of OA gradually increased (2.２0±0.4７ vs. 1.4５±0.27), and in the plasma, lung and kidney 60 minutes after injection of OA gradually increased (plasma (μmol/L): 3.10±0.58 vs. 2.33±0.35, lung (μmol/g): 5.56±1.30 vs. 2.05±0.52, kidney (μmol/g): 1.61±0.27 vs. 0.98±0.42), and in the brain, liver and small intestine 90 minutes after injection of OA gradually increased (brain (μmol/g): 6.78±1.38 vs. 5.83±1.58, liver (μmol/g): 2.58±0.68 vs. 2.11±0.42, small intestine (μmol/g): 2.14±0.51 vs. 0.81±0.26, P<0.05 or P<0.01). ACE activity was reduced in the plasma and lung 60 minutes after injection of OA (plasma (μmol·min-１·L-１): 15.47±1.68 vs. 19.87±3.11, lung(μmol·min-１·g-１): 20.61±1.81 vs. 26.26±1.93), but in the kidney (μmol·min-１·g-１) it was gradually increased (15.92±1.20 vs. 13.67±2.26), and in the small intestine (μmol·min-１·g-１) 90 minutes after injection of OA it gradually increased (4.42±0.34 vs. 3.29±0.24, all P<0.01). Gαq/11 protein expression in the lung and small intestine obviously increased 30 minutes after injection of OA (lung: (119.24±2.38)% vs. (100.00±18.74)%, small intestine: (138.91±23.03)% vs. (100.00±１9.43）%), and in the brain, heart and kidney increased 60 minutes after injection of OA (brain: （141.85±33.82）% vs. (100.00±16.81)%, heart: (124.72±24.0５)% vs. (100.00±16.04)%, kidney: (123.98±25.74)% vs. (100.00±8.50)%), and in the liver increased 90 minutes after injection of OA ((134.34±19.14）％ vs. (100.00±13.04)%, P<0.05 or P<0.0１). A positive correlation between the change in Gαq/11 protein expression and LDH in these organs (r=0.584, P<0.05) was found. Conclusion Up-regulation of Gq/11 protein expression in the lung, brain, heart, kidney, liver and small intestine may induce abnormal activity of phosphatidyl inositol signal transduction and thus plays a role in the production of multiple organ injury during ARDS.
