CAJ | 학술논문

目的探讨盐酸戊乙奎醚对脓毒症大鼠肺组织高迁移率族蛋白B1(HMGB1) mRNA表达的影响.方法雄性Wistar大鼠30只,体质量200～250 g,采用随机数字表法,将其随机分为3组(n=10):假手术组(S组)、脓毒症组(L组)、盐酸戊乙奎醚组(PH组).除S组外,其他2组采用盲肠结扎穿孔术制备大鼠脓毒症诱发急性肺损伤模型.PH组于术毕腹腔注射盐酸戊乙奎醚0.45 mg/kg,S组和L组给予等容量生理盐水.分别于术后24、48h时处死5只大鼠,取肺组织,测定HMGB1 mRNA表达、髓过氧化物酶(MPO)活性和核因子κB(NF-κB)活性,光镜下观察肺组织病理学结果.结果与S组比较,其他2组肺组织HMGB1 mRNA表达上调,MPO活性升高(P＜0.05);与L组比较,PH组肺组织HMGB1 mRNA表达下调,MPO活性降低(P＜0.01).PH组肺组织NF-κB活性逐渐降低,肺组织损伤程度逐渐减轻.结论盐酸戊乙奎醚减轻脓毒症大鼠急性肺损伤的机制与下调肺组织HMGB1基因表达有关,其下调HMGB1基因表达的机制与抑制NF-κB活化有关.
목적 탐토염산무을규미대농독증대서폐조직고천이솔족단백B1(HMGB1) mRNA표체적영향.방법 웅성Wistar대서30지,체질량200～250 g,채용수궤수자표법,장기수궤분위3조(n=10):가수술조(S조)、농독증조(L조)、염산무을규미조(PH조).제S조외,기타2조채용맹장결찰천공술제비대서농독증유발급성폐손상모형.PH조우술필복강주사염산무을규미0.45 mg/kg,S조화L조급여등용량생리염수.분별우술후24、48h시처사5지대서,취폐조직,측정HMGB1 mRNA표체、수과양화물매(MPO)활성화핵인자κB(NF-κB)활성,광경하관찰폐조직병이학결과.결과 여S조비교,기타2조폐조직HMGB1 mRNA표체상조,MPO활성승고(P＜0.05);여L조비교,PH조폐조직HMGB1 mRNA표체하조,MPO활성강저(P＜0.01).PH조폐조직NF-κB활성축점강저,폐조직손상정도축점감경.결론 염산무을규미감경농독증대서급성폐손상적궤제여하조폐조직HMGB1기인표체유관,기하조HMGB1기인표체적궤제여억제NF-κB활화유관.
Objective To investigate the effect of penehyclidine hydrochloride on expression of high mobility group box 1 (HMGB1) mRNA in lung tissue in septic rats.Methods Thirty male Wistar rats weighing 200-250 g were randomly divided into 3 groups (n =10 each):group sham operation (group S),group sepsis(group L),group penehyclidine hydrochloride (groups PH).Sepsis was induced by cecal ligation and puncture in groups L,PH.Penehyclidine Hydrochloride 0.45 mg/kg were injected intraperitoneally at the end of operation in groups PH.Five animals in each group were sacrificed at 24 and 48 h after operation respectively.The lungs were removed for microscopic examination and determination of HMGB1 mRNA expression,MPO activity and activation of NF-κB.Results Sepsis up-regulated HMGB1 mRNA and increased MPO activity and activation of NF-κB and induced lung histopathological damage.Penehyclidine Hydrochloride attenuated the above mentioned sepsis-induced changes in a dosedependent manner.Conclusions Penehyclidine Hydrochloride can attenuate sepsis-induced acute lung injury by down-regulating HMGB1 mRNA expression and inhibiting activation of NF-κB.