中国急救医学
中國急救醫學
중국급구의학
CHINESE JOURNAL OF CRITICAL CARE MEDICINE
2014年
12期
1119-1122
,共4页
急性肺损伤(ALI)%环氧合酶-2(COX-2)%过氧化物酶增殖体激活受体-γ(PPAR-γ)%美洛昔康
急性肺損傷(ALI)%環氧閤酶-2(COX-2)%過氧化物酶增殖體激活受體-γ(PPAR-γ)%美洛昔康
급성폐손상(ALI)%배양합매-2(COX-2)%과양화물매증식체격활수체-γ(PPAR-γ)%미락석강
Acute lung injury(ALI)%Cyclooxygenase-2(COX-2)%Peroxisome proliferation activated receptor -γ( PPAR-γ)%Meloxicam
目的：观察美洛昔康对内毒素（endotoxin， ET）复制急性肺损伤（ALI）时兔肺组织环氧合酶－2（ cyclooxygenase －2， COX －2）和过氧化物酶增殖体激活受体－γ（ peroxisome proliferation activated receptor －γ， PPAR－γ） mRNA变化的影响，来探讨其对ALI保护作用的机制。方法将24只日本大耳白兔随机分为生理盐水对照组（ A组）、内毒素致伤组（ B组）、美洛昔康干预组（C组）。用ET（700μg／kg）静脉注射复制兔子ALI模型，美洛昔康（2．5 mg／kg）进行干预，观测兔动脉血气、光镜肺组织病理、肺组织中COX－2 mRNA与PPAR－γmRNA的表达。结果 COX－2 mRNA 表达 B 组显著高于 A 组（P ＜0．01），C 组显著低于 B 组（P＜0．01）。PPAR－γmRNA表达B组显著低于A组（P＜0．01），C组显著高于B组（P＜0．01）。结论美洛昔康可通过下调COX－2 mRNA和上调PPAR－γmRNA的表达，在一定程度上对兔内毒素性ALI产生保护作用。
目的：觀察美洛昔康對內毒素（endotoxin， ET）複製急性肺損傷（ALI）時兔肺組織環氧閤酶－2（ cyclooxygenase －2， COX －2）和過氧化物酶增殖體激活受體－γ（ peroxisome proliferation activated receptor －γ， PPAR－γ） mRNA變化的影響，來探討其對ALI保護作用的機製。方法將24隻日本大耳白兔隨機分為生理鹽水對照組（ A組）、內毒素緻傷組（ B組）、美洛昔康榦預組（C組）。用ET（700μg／kg）靜脈註射複製兔子ALI模型，美洛昔康（2．5 mg／kg）進行榦預，觀測兔動脈血氣、光鏡肺組織病理、肺組織中COX－2 mRNA與PPAR－γmRNA的錶達。結果 COX－2 mRNA 錶達 B 組顯著高于 A 組（P ＜0．01），C 組顯著低于 B 組（P＜0．01）。PPAR－γmRNA錶達B組顯著低于A組（P＜0．01），C組顯著高于B組（P＜0．01）。結論美洛昔康可通過下調COX－2 mRNA和上調PPAR－γmRNA的錶達，在一定程度上對兔內毒素性ALI產生保護作用。
목적：관찰미락석강대내독소（endotoxin， ET）복제급성폐손상（ALI）시토폐조직배양합매－2（ cyclooxygenase －2， COX －2）화과양화물매증식체격활수체－γ（ peroxisome proliferation activated receptor －γ， PPAR－γ） mRNA변화적영향，래탐토기대ALI보호작용적궤제。방법장24지일본대이백토수궤분위생리염수대조조（ A조）、내독소치상조（ B조）、미락석강간예조（C조）。용ET（700μg／kg）정맥주사복제토자ALI모형，미락석강（2．5 mg／kg）진행간예，관측토동맥혈기、광경폐조직병리、폐조직중COX－2 mRNA여PPAR－γmRNA적표체。결과 COX－2 mRNA 표체 B 조현저고우 A 조（P ＜0．01），C 조현저저우 B 조（P＜0．01）。PPAR－γmRNA표체B조현저저우A조（P＜0．01），C조현저고우B조（P＜0．01）。결론미락석강가통과하조COX－2 mRNA화상조PPAR－γmRNA적표체，재일정정도상대토내독소성ALI산생보호작용。
Objective To investigate the effects of meloxicam on the changes of cyclooxygenase -2(COX-2) and peroxisome proliferation activated receptor -γ(PPAR-γ)mRNA in lung of rabbits with acute lung injury (ALI) induced by endotoxin (ET) and to explore it′s protective mechanism .Methods Twenty four Japanese flap -eared white rabbits were randomly assigned to three groups:control group (A group), ET -treated group(B group) and meloxicam for treatment group (C group).Rabbit ALI models were replicated with intravascular ET injection (700 μg/kg weight), meloxicam (2.5 mg/kg weight) was intravascularly injected as treatment group.During the experiment, arterial blood gases were measured.The pathologic changes were examined with light microscope .We measured COX -2 and PPAR -γmRNA in every group .Results COX -2 mRNA expression in B group was significantly higher than that in A group (P<0.01),and COX-2 mRNA expression in C group was significantly lower than in B group (P<0.01).PPAR-γmRNA expression in B group was significantly lower than that in A group (P<0.01),and PPAR-γmRNA expression in C group was significantly higher than in B group (P<0.01).Conclusion Meloxicam can down -regulate COX-2 and up-regulate PPAR-γexpression , which posseses protective effects on ALI in rabbits induced by ET .
