中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
6期
1329-1332
,共4页
黄晓雷%陈岱莉%齐晓非%曹君%李元涛
黃曉雷%陳岱莉%齊曉非%曹君%李元濤
황효뢰%진대리%제효비%조군%리원도
BML-111%失血性休克%肝脏%炎性反应
BML-111%失血性休剋%肝髒%炎性反應
BML-111%실혈성휴극%간장%염성반응
BML-111%Hemorrhagic shock%Liver%Inflammatory response
目的 观察脂氧素受体激动剂BML-111对大鼠失血性休克诱发的肝功能损伤和炎性反应的影响.方法 将40只雄性SD大鼠随机分为5组:假手术组、失血性休克-复苏组、低剂量BML-111+失血性休克-复苏组、中剂量BML-111+失血性休克-复苏组、高剂量BML-111+失血性休克-复苏组.全自动生化分析仪检测血浆中肝功能相关指标.酶联免疫吸附试验(ELISA)法检测肝组织诱导型一氧化氮合酶(iNOS)及内皮素-1(ET-1)表达水平.Western blot法检测肝组织胞质p65、κB抑制蛋白(IκB)-α、肿瘤坏死因子-α(TNF-α)及胞核p65蛋白表达水平.结果 0.5、1.0、2.0 mg/kg BML-111分别使失血性休克复苏大鼠血浆谷丙转氨酶(ALT)水平下降22.7％、37.1％和46.1％(P＜0.05);0.5、1.0、2.0 mg/kg BML-111分别使失血性休克复苏大鼠血浆谷草转氨酶(AST)水平下降40.6％、52.7％和60.9％ (P ＜0.05);0.5、1.0、2.0 mg/kg BML-111分别使失血性休克复苏大鼠血浆乳酸脱氢酶(LDH)水平下降39.4％、46.4％和58.2％ (P ＜0.05).同时,BML-111缓解失血性休克-复苏大鼠肝脏iNOS和ET-1表达水平升高和核因子-κB (NF-κB)-p65信号通路激活(P＜0.05).结论 脂氧素受体激动剂BML-111可通过抑制NF-κB-p65缓解大鼠失血性休克复苏后肝脏损伤和炎性反应.
目的 觀察脂氧素受體激動劑BML-111對大鼠失血性休剋誘髮的肝功能損傷和炎性反應的影響.方法 將40隻雄性SD大鼠隨機分為5組:假手術組、失血性休剋-複囌組、低劑量BML-111+失血性休剋-複囌組、中劑量BML-111+失血性休剋-複囌組、高劑量BML-111+失血性休剋-複囌組.全自動生化分析儀檢測血漿中肝功能相關指標.酶聯免疫吸附試驗(ELISA)法檢測肝組織誘導型一氧化氮閤酶(iNOS)及內皮素-1(ET-1)錶達水平.Western blot法檢測肝組織胞質p65、κB抑製蛋白(IκB)-α、腫瘤壞死因子-α(TNF-α)及胞覈p65蛋白錶達水平.結果 0.5、1.0、2.0 mg/kg BML-111分彆使失血性休剋複囌大鼠血漿穀丙轉氨酶(ALT)水平下降22.7％、37.1％和46.1％(P＜0.05);0.5、1.0、2.0 mg/kg BML-111分彆使失血性休剋複囌大鼠血漿穀草轉氨酶(AST)水平下降40.6％、52.7％和60.9％ (P ＜0.05);0.5、1.0、2.0 mg/kg BML-111分彆使失血性休剋複囌大鼠血漿乳痠脫氫酶(LDH)水平下降39.4％、46.4％和58.2％ (P ＜0.05).同時,BML-111緩解失血性休剋-複囌大鼠肝髒iNOS和ET-1錶達水平升高和覈因子-κB (NF-κB)-p65信號通路激活(P＜0.05).結論 脂氧素受體激動劑BML-111可通過抑製NF-κB-p65緩解大鼠失血性休剋複囌後肝髒損傷和炎性反應.
목적 관찰지양소수체격동제BML-111대대서실혈성휴극유발적간공능손상화염성반응적영향.방법 장40지웅성SD대서수궤분위5조:가수술조、실혈성휴극-복소조、저제량BML-111+실혈성휴극-복소조、중제량BML-111+실혈성휴극-복소조、고제량BML-111+실혈성휴극-복소조.전자동생화분석의검측혈장중간공능상관지표.매련면역흡부시험(ELISA)법검측간조직유도형일양화담합매(iNOS)급내피소-1(ET-1)표체수평.Western blot법검측간조직포질p65、κB억제단백(IκB)-α、종류배사인자-α(TNF-α)급포핵p65단백표체수평.결과 0.5、1.0、2.0 mg/kg BML-111분별사실혈성휴극복소대서혈장곡병전안매(ALT)수평하강22.7％、37.1％화46.1％(P＜0.05);0.5、1.0、2.0 mg/kg BML-111분별사실혈성휴극복소대서혈장곡초전안매(AST)수평하강40.6％、52.7％화60.9％ (P ＜0.05);0.5、1.0、2.0 mg/kg BML-111분별사실혈성휴극복소대서혈장유산탈경매(LDH)수평하강39.4％、46.4％화58.2％ (P ＜0.05).동시,BML-111완해실혈성휴극-복소대서간장iNOS화ET-1표체수평승고화핵인자-κB (NF-κB)-p65신호통로격활(P＜0.05).결론 지양소수체격동제BML-111가통과억제NF-κB-p65완해대서실혈성휴극복소후간장손상화염성반응.
Objective To investigate the effects of BML-111 on liver injury and inflammatory responses after hemorrhagic shock and resuscitation in rats.Methods Forty male SD rats were randomly divided into 5 groups:sham group,hemorrhagic shock-resuscitation (HS-R) group and BML1111-3 group.The serum liver function-related index was monitored by automatic biochemical analyzer.Liver protein levels of inducible nitric oxide synthase (iNOS) and endothelin-1 (ET-1) were detected by enzyme linked immunosorbent assay (ELISA).The protein levels of cytoplasmic p65,inhibitory κB (IκB)-α,tumor necrosis factor-α (TNF-α) and nuclear p65 were detected by Western blotting.Results As compared with HS-R group,0.5,1.0 and 2.0 mg/kg of BML-111 treatments respectively decreased serum alanine transaminase (ALT) levels by 22.7％,37.1％ and 46.1％ respectively after hemorrhagic shock and resuscitation (P ＜ 0.05).As compared with hemorrhagic shock-resuscitation group,0.5,1.0 and 2.0 mg/kg of BML-111 treatments respectively decreased serum aspartate aminotransferase (AST) levels by 40.6％,52.7％ and 60.9％ respectively after hemorrhagic shock and resuscitation (P ＜0.05).As compared with hemorrhagic shock-resuscitation group,0.5,1.0 and 2.0 mg/kg of BML-111 treatments respectively decreased serum lactate dehydrogenase (LDH) levels by 39.4％,46.4％ and 58.2％ respectively after hemorrhagic shock and resuscitation (P ＜ 0.05).Additionally,treatments of BML-111 also decreased hepatic levels of iNOS and ET-1,and attenuated the activation of hepatic NF-κB-p65 signaling pathway after hemorrhagic shock and resuscitation (P ＜ 0.05).Conclusion BML-111 can attenuate liver injury and inflammatory responses after hemorrhagic shock and resuscitation by inhibiting NF-κB-p65 signaling pathway.
