中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
1期
112-115
,共4页
蔡朦朦%鲍红光%斯妍娜%徐丽%韩流%施韬%王宏宇%谢欣怡
蔡朦朦%鮑紅光%斯妍娜%徐麗%韓流%施韜%王宏宇%謝訢怡
채몽몽%포홍광%사연나%서려%한류%시도%왕굉우%사흔이
脂联素%脓毒症%中性白细胞浸润%抗原,CD11b%呼吸爆发
脂聯素%膿毒癥%中性白細胞浸潤%抗原,CD11b%呼吸爆髮
지련소%농독증%중성백세포침윤%항원,CD11b%호흡폭발
Adiponectin%Sepsis%Neutrophil infiltration%Antigens,CD11b%Respiratory burst
目的 评价脂联素(APN)预先给药对脓毒症大鼠外周血中性粒细胞CD11b表达和呼吸氧爆发水平的影响.方法 清洁级健康雄性SD大鼠72只,10~ 14周龄,体重250 ~ 300 g,采用随机数字表法,将其分为3组(n=24):对照组(C组)、脓毒症模型组(CLP组)和APN预先给药组(APN组).CLP组和APN组采用盲肠结扎穿孔法建立脓毒症模型,APN组于CLP术前12 h时腹腔注射基因重组APN 6 mg/kg.于术后6、12和24h时每组随机抽取8只大鼠,经眼眶静脉丛采血0.8 ml,采用流式细胞分析术检测外周血中性粒细胞CD11b的表达和呼吸氧爆发水平,膜联蛋白Annexin-V/碘化丙啶双染法检测中性粒细胞凋亡率,于术后24h时处死大鼠取肺组织,检测肺组织MPO活性.另取30只大鼠,每组10只,作相应处理后,记录术后7d的生存情况.结果 与C组比较,CLP组和APN组中性粒细胞CD11b表达上调,呼吸氧爆发水平、肺组织MPO活性升高,中性粒细胞凋亡率及术后7d生存率降低(P<0.05);与CLP组比较,APN组中性粒细胞CD11b表达及呼吸氧爆发水平和肺组织MPO活性降低,术后6h时中性粒细胞凋亡率及术后7d生存率升高(P<0.05).结论 APN预先给药可减轻脓毒症大鼠炎性反应,其机制可能与抑制脓毒症时过度激活的中性粒细胞黏附分子CD11b的表达、呼吸氧爆发水平及促进中性粒细胞凋亡有关.
目的 評價脂聯素(APN)預先給藥對膿毒癥大鼠外週血中性粒細胞CD11b錶達和呼吸氧爆髮水平的影響.方法 清潔級健康雄性SD大鼠72隻,10~ 14週齡,體重250 ~ 300 g,採用隨機數字錶法,將其分為3組(n=24):對照組(C組)、膿毒癥模型組(CLP組)和APN預先給藥組(APN組).CLP組和APN組採用盲腸結扎穿孔法建立膿毒癥模型,APN組于CLP術前12 h時腹腔註射基因重組APN 6 mg/kg.于術後6、12和24h時每組隨機抽取8隻大鼠,經眼眶靜脈叢採血0.8 ml,採用流式細胞分析術檢測外週血中性粒細胞CD11b的錶達和呼吸氧爆髮水平,膜聯蛋白Annexin-V/碘化丙啶雙染法檢測中性粒細胞凋亡率,于術後24h時處死大鼠取肺組織,檢測肺組織MPO活性.另取30隻大鼠,每組10隻,作相應處理後,記錄術後7d的生存情況.結果 與C組比較,CLP組和APN組中性粒細胞CD11b錶達上調,呼吸氧爆髮水平、肺組織MPO活性升高,中性粒細胞凋亡率及術後7d生存率降低(P<0.05);與CLP組比較,APN組中性粒細胞CD11b錶達及呼吸氧爆髮水平和肺組織MPO活性降低,術後6h時中性粒細胞凋亡率及術後7d生存率升高(P<0.05).結論 APN預先給藥可減輕膿毒癥大鼠炎性反應,其機製可能與抑製膿毒癥時過度激活的中性粒細胞黏附分子CD11b的錶達、呼吸氧爆髮水平及促進中性粒細胞凋亡有關.
목적 평개지련소(APN)예선급약대농독증대서외주혈중성립세포CD11b표체화호흡양폭발수평적영향.방법 청길급건강웅성SD대서72지,10~ 14주령,체중250 ~ 300 g,채용수궤수자표법,장기분위3조(n=24):대조조(C조)、농독증모형조(CLP조)화APN예선급약조(APN조).CLP조화APN조채용맹장결찰천공법건립농독증모형,APN조우CLP술전12 h시복강주사기인중조APN 6 mg/kg.우술후6、12화24h시매조수궤추취8지대서,경안광정맥총채혈0.8 ml,채용류식세포분석술검측외주혈중성립세포CD11b적표체화호흡양폭발수평,막련단백Annexin-V/전화병정쌍염법검측중성립세포조망솔,우술후24h시처사대서취폐조직,검측폐조직MPO활성.령취30지대서,매조10지,작상응처리후,기록술후7d적생존정황.결과 여C조비교,CLP조화APN조중성립세포CD11b표체상조,호흡양폭발수평、폐조직MPO활성승고,중성립세포조망솔급술후7d생존솔강저(P<0.05);여CLP조비교,APN조중성립세포CD11b표체급호흡양폭발수평화폐조직MPO활성강저,술후6h시중성립세포조망솔급술후7d생존솔승고(P<0.05).결론 APN예선급약가감경농독증대서염성반응,기궤제가능여억제농독증시과도격활적중성립세포점부분자CD11b적표체、호흡양폭발수평급촉진중성립세포조망유관.
Objective To investigate the effects of adiponectin (APN) pretreatment on the peripheral blood polymorphonuclear leucocyte (PMN) CD1 1b expression and respiratory burst activity in septic rats.Methods Seventy-two male Sprague-Dawley rats,weighing 250-300 g,were randomly allocated into 3 groups (n =24 each) using a random number table:control group (C group),cecal ligation and puncture (CLP) group and APN pretreatment group (APN group).Sepsis was induced by CLP in CLP and APN groups.In APN group,recombinant adiponectin 6 mg/kg was injected intraperitoneally at 12 h before CLP.Eight rats in each group were randomly chosen at 6,12 and 24 h after operation to collect venous blood samples for measurement of the peripheral blood PMN CD11 b expression and respiratory burst activity with flow cytometry.The apoptosis rate was detected with Annexin-V/PI double staining.The animals were sacrificed at 24 h after operation and pulmonary specimens were obtained to detect myeloperoxidase (MPO) activity in lung tissues.Another 10 rats in each group were chosen and treated according to the method mentioned above,and the survival rates within 7 days after operation were observed in the three groups.Results Compared with C group,the expression of CD11b on PMNs was significantly up-regulated,the PMN respiratory burst activity and MPO activity were increased,and the apoptosis rate and survival rate within 7 days after operation were decreased in CLP group (P < 0.05).Compared with CLP group,the expression of CD11b on PMNs,PMN respiratory burst activity and MPO activity were significantly decreased,and the apoptosis rate of PMNs at 6 h after the operation and survival rate within 7 days after operation were increased in APN group (P < 0.05).Conclusion Adiponectin pretreatment can attenuate sepsis-induced inflammatory responses and the mechanism may be related to inhibition of excessively activated PMN adhesion CD11b expression during sepsis and respiratory burst activity and promotion of apoptosis in rat PMNs.