中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
8期
1004-1006
,共3页
刘薇%严虹%李季玉%陈璟莉%严启韬
劉薇%嚴虹%李季玉%陳璟莉%嚴啟韜
류미%엄홍%리계옥%진경리%엄계도
环AMP%葡甲胺%呼吸窘迫综合征,成人%内毒素血症
環AMP%葡甲胺%呼吸窘迫綜閤徵,成人%內毒素血癥
배AMP%포갑알%호흡군박종합정,성인%내독소혈증
Cyclic AMP%Meglumine%Respiratory distress syndrome,adult%Endotoxemia
目的 探讨环磷酸腺苷葡甲胺预先给药对内毒素(LPS)致大鼠急性肺损伤(ALI)的影响.方法 健康成年雄性SD大鼠54只,2～3月龄,体重200 ～ 250 g,采用随机数字表法,将其分为3组(n=18):对照组(C组)、LPS组和环磷酸腺苷葡甲胺预先给药组(MCA组).LPS组和MCA组股静脉注射LPS 10 mg/kg制备大鼠ALI模型,C组注射等容量生理盐水.MCA组于LPS注射前20 min时股静脉注射环磷酸腺苷葡甲胺2 mg/kg,C组和LPS组注射等容量生理盐水.于LPS注射前即刻、注射后2和4h时各取6只大鼠,采集腹主动脉血样行血气分析,记录PaO2和PaCO2,采用ELISA法测定血浆TNF-α和IL-10浓度.于LPS注射后4h时处死6只大鼠,取肺组织,电镜下观察病理学改变,采用ELISA法测定环磷酸腺苷(cAMP)的活性,采用Western blot法检测核蛋白NF-κB p65表达水平.结果 与C组比较,LPS组PaO2和肺组织cAMP活性降低,PaCO2、血浆TNF-α和IL-10的浓度及肺组织核蛋白NF-κB p65表达水平升高(P＜0.05).与LPS组比较,MCA组PaO2、肺组织cAMP活性与血浆IL-10浓度升高,PaCO2、血浆TNF-α浓度和肺组织核蛋白NF-κB p65表达水平降低(P＜0.05),病理学损伤减轻.结论 环磷酸腺苷葡甲胺预先给药可减轻LPS致大鼠ALI,其机制可能与增强肺组织细胞内cAMP水平,激活cAMP信号通路,抑制NF-κB活性,减轻炎性反应有关.
目的 探討環燐痠腺苷葡甲胺預先給藥對內毒素(LPS)緻大鼠急性肺損傷(ALI)的影響.方法 健康成年雄性SD大鼠54隻,2～3月齡,體重200 ～ 250 g,採用隨機數字錶法,將其分為3組(n=18):對照組(C組)、LPS組和環燐痠腺苷葡甲胺預先給藥組(MCA組).LPS組和MCA組股靜脈註射LPS 10 mg/kg製備大鼠ALI模型,C組註射等容量生理鹽水.MCA組于LPS註射前20 min時股靜脈註射環燐痠腺苷葡甲胺2 mg/kg,C組和LPS組註射等容量生理鹽水.于LPS註射前即刻、註射後2和4h時各取6隻大鼠,採集腹主動脈血樣行血氣分析,記錄PaO2和PaCO2,採用ELISA法測定血漿TNF-α和IL-10濃度.于LPS註射後4h時處死6隻大鼠,取肺組織,電鏡下觀察病理學改變,採用ELISA法測定環燐痠腺苷(cAMP)的活性,採用Western blot法檢測覈蛋白NF-κB p65錶達水平.結果 與C組比較,LPS組PaO2和肺組織cAMP活性降低,PaCO2、血漿TNF-α和IL-10的濃度及肺組織覈蛋白NF-κB p65錶達水平升高(P＜0.05).與LPS組比較,MCA組PaO2、肺組織cAMP活性與血漿IL-10濃度升高,PaCO2、血漿TNF-α濃度和肺組織覈蛋白NF-κB p65錶達水平降低(P＜0.05),病理學損傷減輕.結論 環燐痠腺苷葡甲胺預先給藥可減輕LPS緻大鼠ALI,其機製可能與增彊肺組織細胞內cAMP水平,激活cAMP信號通路,抑製NF-κB活性,減輕炎性反應有關.
목적 탐토배린산선감포갑알예선급약대내독소(LPS)치대서급성폐손상(ALI)적영향.방법 건강성년웅성SD대서54지,2～3월령,체중200 ～ 250 g,채용수궤수자표법,장기분위3조(n=18):대조조(C조)、LPS조화배린산선감포갑알예선급약조(MCA조).LPS조화MCA조고정맥주사LPS 10 mg/kg제비대서ALI모형,C조주사등용량생리염수.MCA조우LPS주사전20 min시고정맥주사배린산선감포갑알2 mg/kg,C조화LPS조주사등용량생리염수.우LPS주사전즉각、주사후2화4h시각취6지대서,채집복주동맥혈양행혈기분석,기록PaO2화PaCO2,채용ELISA법측정혈장TNF-α화IL-10농도.우LPS주사후4h시처사6지대서,취폐조직,전경하관찰병이학개변,채용ELISA법측정배린산선감(cAMP)적활성,채용Western blot법검측핵단백NF-κB p65표체수평.결과 여C조비교,LPS조PaO2화폐조직cAMP활성강저,PaCO2、혈장TNF-α화IL-10적농도급폐조직핵단백NF-κB p65표체수평승고(P＜0.05).여LPS조비교,MCA조PaO2、폐조직cAMP활성여혈장IL-10농도승고,PaCO2、혈장TNF-α농도화폐조직핵단백NF-κB p65표체수평강저(P＜0.05),병이학손상감경.결론 배린산선감포갑알예선급약가감경LPS치대서ALI,기궤제가능여증강폐조직세포내cAMP수평,격활cAMP신호통로,억제NF-κB활성,감경염성반응유관.
Objective To evaluate the effects of meglumine cyclic adenylate (MCA) pretreatment on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in rats.Methods Fifty-four adult male Sprague Dawley rats,aged 2-3 months,weighing 200-250 g,were randomly divided into 3 groups (n =18 each) using a random number table:control group (group C),ALI group and MCA pretreatment group (group MCA).ALI was induced with LPS 10 mg/kg injected via the femoral vein in ALI and MCA groups.In group MCA,MCA 2 mg/kg was injected via the femoral vein at 20 min before LPS injection,while the equal volume of normal saline was given in C and LPS groups.Immediately before LPS injection and at 2 and 4 h after LPS injection,the blood samples were taken from the abdominal aorta for determination of PaO2,PaCO2 and plasma concentrations of tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10).Six rats were sacrificed at 4 h after LPS injection and pulmonary specimens were obtained for microscopic examination of the pathological changes and for determination of cyclic adenosine monophosphate (cAMP) activity (by ELISA) and NF-κB p65 expression in nucleus (by Western blot).Results Compared with group C,PaO2 and cAMP activity in lung tissues were significantly decreased,and PaCO2,plasma concentrations of IL-10 and TNF-α and NF-κB p65 expression in nucleus in lung tissues were increased in group LPS.Compared with group LPS,PaO2,cAMP activity in lung tissues and plasma concentrations of IL-10 were significantly increased,and PaCO2,plasma concentration of TNF-α and NF-κB p65 expression in nucleus in lung tissues were decreased and the pathologic changes of lungs were attenuated in group MCA.Conclusion MCA pretreatment can attenuate ALI induced by LPS,and the mechanism is related to increased level of cAMP,activated cAMP signaling pathway,inhibited NF-κB activity and reduced inflammatory responses in lung tissues of rats.
