天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
10期
992-994
,共3页
邢志伟%张建武%梁玉庚%吕翠环%杜月菊%刘锐%孙红梅
邢誌偉%張建武%樑玉庚%呂翠環%杜月菊%劉銳%孫紅梅
형지위%장건무%량옥경%려취배%두월국%류예%손홍매
急性肺损伤%NF-κB%一氧化氮合酶%环氧化酶2抑制剂%环氧化酶2
急性肺損傷%NF-κB%一氧化氮閤酶%環氧化酶2抑製劑%環氧化酶2
급성폐손상%NF-κB%일양화담합매%배양화매2억제제%배양화매2
acute lung injury%NF-κB%nitric oxide synthase%cyclooxygenase 2 inhibitors%cyclooxygenase 2
目的探讨脂多糖（LPS）所致大鼠急性肺损伤时环氧化酶-2（COX-2）抑制剂塞来昔布对肺组织的核因子-κB（NF-κB）p65和诱导型一氧化氮合酶（iNOS）表达的影响。方法将60只大鼠随机分为对照组、LPS组、治疗组和塞来昔布组，每组15只。LPS组尾静脉注射LPS（5 mg/kg）复制急性肺损伤模型；治疗组注射LPS复制急性肺损伤模型后30 min用塞来昔布灌胃（20 mg/kg）；塞来昔布组不造模，于相同时间点用相同剂量塞来昔布灌胃；对照组不造模、不给药，给等量的生理盐水；各组均于3 h后放血处死动物。采用蛋白质印迹（Western blot）和逆转录-聚合酶链反应（RT-PCR）方法分别检测肺组织COX-2、NF-κB p65、iNOS蛋白及NF-κB p65、iNOS mRNA的表达。结果LPS组与对照组相比COX-2、NF-κB p65和iNOS蛋白及NF-κB p65、iNOS mRNA表达均显著升高（P<0.01）；治疗组NF-κB p65、iNOS mRNA和蛋白表达较LPS组明显降低（P<0.01）。结论选择性COX-2抑制剂塞来昔布对急性肺损伤大鼠有保护作用。
目的探討脂多糖（LPS）所緻大鼠急性肺損傷時環氧化酶-2（COX-2）抑製劑塞來昔佈對肺組織的覈因子-κB（NF-κB）p65和誘導型一氧化氮閤酶（iNOS）錶達的影響。方法將60隻大鼠隨機分為對照組、LPS組、治療組和塞來昔佈組，每組15隻。LPS組尾靜脈註射LPS（5 mg/kg）複製急性肺損傷模型；治療組註射LPS複製急性肺損傷模型後30 min用塞來昔佈灌胃（20 mg/kg）；塞來昔佈組不造模，于相同時間點用相同劑量塞來昔佈灌胃；對照組不造模、不給藥，給等量的生理鹽水；各組均于3 h後放血處死動物。採用蛋白質印跡（Western blot）和逆轉錄-聚閤酶鏈反應（RT-PCR）方法分彆檢測肺組織COX-2、NF-κB p65、iNOS蛋白及NF-κB p65、iNOS mRNA的錶達。結果LPS組與對照組相比COX-2、NF-κB p65和iNOS蛋白及NF-κB p65、iNOS mRNA錶達均顯著升高（P<0.01）；治療組NF-κB p65、iNOS mRNA和蛋白錶達較LPS組明顯降低（P<0.01）。結論選擇性COX-2抑製劑塞來昔佈對急性肺損傷大鼠有保護作用。
목적탐토지다당（LPS）소치대서급성폐손상시배양화매-2（COX-2）억제제새래석포대폐조직적핵인자-κB（NF-κB）p65화유도형일양화담합매（iNOS）표체적영향。방법장60지대서수궤분위대조조、LPS조、치료조화새래석포조，매조15지。LPS조미정맥주사LPS（5 mg/kg）복제급성폐손상모형；치료조주사LPS복제급성폐손상모형후30 min용새래석포관위（20 mg/kg）；새래석포조불조모，우상동시간점용상동제량새래석포관위；대조조불조모、불급약，급등량적생리염수；각조균우3 h후방혈처사동물。채용단백질인적（Western blot）화역전록-취합매련반응（RT-PCR）방법분별검측폐조직COX-2、NF-κB p65、iNOS단백급NF-κB p65、iNOS mRNA적표체。결과LPS조여대조조상비COX-2、NF-κB p65화iNOS단백급NF-κB p65、iNOS mRNA표체균현저승고（P<0.01）；치료조NF-κB p65、iNOS mRNA화단백표체교LPS조명현강저（P<0.01）。결론선택성COX-2억제제새래석포대급성폐손상대서유보호작용。
Objective To investigate the effects of celecoxib on the expressions of nuclear factor-κB (NF-κB) p65 and inducible nitric oxide synthase (iNOS) in rat model of acute lung injury induced by lipopolysaccharide (LPS). Methods Sixty rats were randomly divided into control group, LPS group, treatment group and celecoxib group (15 rats for each group). To copy the rat model of acute lung injury, LPS(5 mg/kg)was injected into the tail vein in LPS group. Celecoxib (20 mg/kg) was administered by gavage after 30-minute modeling in treatment group. Celecoxib (20 mg/kg)was also administered by ga-vage in celecoxib group. The same volume of normal saline was treated in control group. Rats were sacrificed after 3 h in four groups. The expressions of cyclooxygenase-2 (COX-2), NF-κB p65 and iNOS protein were detected by Western blot analy-sis. The expressions of NF-κB p65 and iNOS mRNA were evaluated by reverse transcription polymerase chain reaction (RT-PCR) assay. Results Compared with control group, expression levels of COX-2, NF-κB p65, iNOS protein,NF-κB p65 and iNOS mRNA were significantly higher in LPS group (P<0.01). The NF-κB p65, iNOS mRNA and protein expressions were significantly decreased in treatment group than those of LPS group (P<0.01). Conclusion The selective COX-2 in-hibitor celecoxib has a protective effect on acute lung injury in rats.
