中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2012年
6期
327-329
,共3页
陈传希%欧阳彬%赖箭波%邱春芳%管向东
陳傳希%歐暘彬%賴箭波%邱春芳%管嚮東
진전희%구양빈%뢰전파%구춘방%관향동
内毒素血症%肠屏障%c-Jun蛋白氨基末端激酶信号通路%D-乳酸
內毒素血癥%腸屏障%c-Jun蛋白氨基末耑激酶信號通路%D-乳痠
내독소혈증%장병장%c-Jun단백안기말단격매신호통로%D-유산
Endotoxemia%Intestinal barrier%c-Jun N-terminal kinase%D-lactate
目的 探讨阻断细胞质内应激信号通路c-Jun蛋白氨基末端激酶(JNK)对内毒素血症大鼠肠屏障损伤的保护作用.方法 24只雄性SD大鼠,按随机数字表法分为对照组、内毒素血症模型组、JNK抑制剂组3组,每组8只.对照组仅给予生理盐水2 ml/kg+JNK抑制剂SP600125的溶剂PPCES液2.5 ml/kg；内毒素血症模型组静脉注射脂多糖( LPS) 10 mg/kg+PPCES液2.5 ml/kg;JNK抑制剂组静脉注射LPS 10 mg/kg+JNK抑制剂SP600125 10 mg/kg.记录各组大鼠活动和生存情况；并于12h后取大鼠同肠,光镜下观察肠道黏膜病理改变；同时取血,采用酶联免疫吸附试验( ELISA)测定血浆D-乳酸含量.结果 对照组大鼠活动正常,无死亡；模型组大鼠精神萎靡、活动减少,12h内死亡1只；JNK抑制剂组大鼠活动较模型组活跃,无死亡.回肠黏膜病理检查显示:与对照组相比,模型组大鼠回肠组织黏膜水肿,绒毛缩短,炎性细胞浸润；INK抑制剂组回肠组织病变较模型组减轻.模型组大鼠血浆D-乳酸含量(μg/L)较对照组显著升高(943.8±439.6比227.9±130.0,P＜0.05)；JNK抑制剂能显著降低内毒素血症大鼠血浆D-乳酸含量(637.4±114.4比943.8±439.6,P＜0.05).结论 抑制细胞质内应激信号通路JNK能减轻内毒素血症大鼠肠屏障损伤.
目的 探討阻斷細胞質內應激信號通路c-Jun蛋白氨基末耑激酶(JNK)對內毒素血癥大鼠腸屏障損傷的保護作用.方法 24隻雄性SD大鼠,按隨機數字錶法分為對照組、內毒素血癥模型組、JNK抑製劑組3組,每組8隻.對照組僅給予生理鹽水2 ml/kg+JNK抑製劑SP600125的溶劑PPCES液2.5 ml/kg；內毒素血癥模型組靜脈註射脂多糖( LPS) 10 mg/kg+PPCES液2.5 ml/kg;JNK抑製劑組靜脈註射LPS 10 mg/kg+JNK抑製劑SP600125 10 mg/kg.記錄各組大鼠活動和生存情況；併于12h後取大鼠同腸,光鏡下觀察腸道黏膜病理改變；同時取血,採用酶聯免疫吸附試驗( ELISA)測定血漿D-乳痠含量.結果 對照組大鼠活動正常,無死亡；模型組大鼠精神萎靡、活動減少,12h內死亡1隻；JNK抑製劑組大鼠活動較模型組活躍,無死亡.迴腸黏膜病理檢查顯示:與對照組相比,模型組大鼠迴腸組織黏膜水腫,絨毛縮短,炎性細胞浸潤；INK抑製劑組迴腸組織病變較模型組減輕.模型組大鼠血漿D-乳痠含量(μg/L)較對照組顯著升高(943.8±439.6比227.9±130.0,P＜0.05)；JNK抑製劑能顯著降低內毒素血癥大鼠血漿D-乳痠含量(637.4±114.4比943.8±439.6,P＜0.05).結論 抑製細胞質內應激信號通路JNK能減輕內毒素血癥大鼠腸屏障損傷.
목적 탐토조단세포질내응격신호통로c-Jun단백안기말단격매(JNK)대내독소혈증대서장병장손상적보호작용.방법 24지웅성SD대서,안수궤수자표법분위대조조、내독소혈증모형조、JNK억제제조3조,매조8지.대조조부급여생리염수2 ml/kg+JNK억제제SP600125적용제PPCES액2.5 ml/kg；내독소혈증모형조정맥주사지다당( LPS) 10 mg/kg+PPCES액2.5 ml/kg;JNK억제제조정맥주사LPS 10 mg/kg+JNK억제제SP600125 10 mg/kg.기록각조대서활동화생존정황；병우12h후취대서동장,광경하관찰장도점막병리개변；동시취혈,채용매련면역흡부시험( ELISA)측정혈장D-유산함량.결과 대조조대서활동정상,무사망；모형조대서정신위미、활동감소,12h내사망1지；JNK억제제조대서활동교모형조활약,무사망.회장점막병리검사현시:여대조조상비,모형조대서회장조직점막수종,융모축단,염성세포침윤；INK억제제조회장조직병변교모형조감경.모형조대서혈장D-유산함량(μg/L)교대조조현저승고(943.8±439.6비227.9±130.0,P＜0.05)；JNK억제제능현저강저내독소혈증대서혈장D-유산함량(637.4±114.4비943.8±439.6,P＜0.05).결론 억제세포질내응격신호통로JNK능감경내독소혈증대서장병장손상.
Objective To examine the protective effects of inhibition of c-Jun N-terminal kinase (JNK) stress signal pathway on the injured intestinal barrier in endotoxemic rats.Methods Twenty-four male Sprague Dwaley (SD) rats were randomly divided into control group,endotoxemia model group and JNK inhibitor group (n=8 each ) to receive administration of:① normal saline 2 m l/kg + PPCES 2.5 ml/kg [ vehicle of JN K inhibitor (SP600125),control group]; ②lipopolysaccharide (LPS) 10 mg/kg + PPCES 2.5 ml/kg (endotoxemia model group); ③LPS 10 mg/kg + JNK inhibitor (SP600125) 10 mg/kg (JNK inhibitor group).The activity and survival rate of the rats were recorded.Ileum tissue samples were collected 12 hours after drug administration for pathological examination.Blood samples were collected at the same time for determination of concentration of D-lactate by enzyme linked immunosorbent assay ( ELISA ).Results Rats in control group were active normally,and there was no death.The endotoxemic rats became lethargic and the activity was reduced,and a rat died within 12 hours after LPS injection.JNK inhibitor improved the general status and activity of the rats,and there was no death.Pathological examination showed there was edema of ileal mucosa,and shortening of villus and inflammatory cell infiltration in model group as compared with control group.JNK inhibitor greatly ameliorated the lesions compared with model group.The concentration of D-lactate (μg/L) in model group was significantly higher than that in control group (943.8 ± 439.6 vs.227.9 ± 130.0,P＜0.05 ).JNK inhibitor could decrease the plasma D-lactate concentration (637.4 ± 114.4 vs.943.8 ±439.6,P＜0.05).Conclusion Inhibition of the JNK stress signal pathway could attenuate the intestinal barrier injury in endotoxemic rats.
