中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
2期
237-239
,共3页
陈龙%成勤%陈西艳%张岩%张茂银%张稳稳%刘功俭%左明章
陳龍%成勤%陳西豔%張巖%張茂銀%張穩穩%劉功儉%左明章
진룡%성근%진서염%장암%장무은%장은은%류공검%좌명장
JNK丝裂原活化蛋白激酶类%内毒素血症%呼吸窘迫综合征,成人
JNK絲裂原活化蛋白激酶類%內毒素血癥%呼吸窘迫綜閤徵,成人
JNK사렬원활화단백격매류%내독소혈증%호흡군박종합정,성인
JNK mitogen-activated protein kinases%Endotoxemia%Respiratory distress syndrome,adult
目的 评价c-Jun氨基末端激酶(JNK)在大鼠内毒素性急性肺损伤中的作用.方法 雄性成年SD大鼠80只,体重250～300 g,采用随机数字表法,将其随机分为4组(n=20):对照组(C组)、急性肺损伤组(ALI组)、SP600125组(S组)和二甲基亚砜组(D组).ALI组、S组和D组尾静脉注射LPS 5 mg/kg,C组尾静脉注射等容量生理盐水;S组和D组给予LPS后,分别尾静脉注射JNK抑制剂SP600125 30 mg/kg或二甲基亚砜0.2 ml.于给予LPS后4 h时,各组处死10只大鼠,回收支气管肺泡灌洗液(BALF)并取肺组织,采用ELISA法检测BALF中TNF-α和IL-1β的浓度,计算肺组织湿重/干重比(W/D比),观察肺组织病理学结果,并进行肺损伤评分.各组其余10只大鼠观察至给予LPS后48 h,记录大鼠生存情况.结果 与C组比较,其余各组BALF中TNF-α和IL-1β的浓度、肺组织W/D比和肺损伤评分升高,生存率降低(P<0.05或0.01);与ALI组比较,S组BALF中TNF-α和IL-1度、肺组织W/D比和肺损伤评分降低,生存率升高(P<0.01),D组差异无统计学意义(P>0.05).结论 JNK的活化参与了大鼠内毒素性急性肺损伤的发生发展.
目的 評價c-Jun氨基末耑激酶(JNK)在大鼠內毒素性急性肺損傷中的作用.方法 雄性成年SD大鼠80隻,體重250～300 g,採用隨機數字錶法,將其隨機分為4組(n=20):對照組(C組)、急性肺損傷組(ALI組)、SP600125組(S組)和二甲基亞砜組(D組).ALI組、S組和D組尾靜脈註射LPS 5 mg/kg,C組尾靜脈註射等容量生理鹽水;S組和D組給予LPS後,分彆尾靜脈註射JNK抑製劑SP600125 30 mg/kg或二甲基亞砜0.2 ml.于給予LPS後4 h時,各組處死10隻大鼠,迴收支氣管肺泡灌洗液(BALF)併取肺組織,採用ELISA法檢測BALF中TNF-α和IL-1β的濃度,計算肺組織濕重/榦重比(W/D比),觀察肺組織病理學結果,併進行肺損傷評分.各組其餘10隻大鼠觀察至給予LPS後48 h,記錄大鼠生存情況.結果 與C組比較,其餘各組BALF中TNF-α和IL-1β的濃度、肺組織W/D比和肺損傷評分升高,生存率降低(P<0.05或0.01);與ALI組比較,S組BALF中TNF-α和IL-1度、肺組織W/D比和肺損傷評分降低,生存率升高(P<0.01),D組差異無統計學意義(P>0.05).結論 JNK的活化參與瞭大鼠內毒素性急性肺損傷的髮生髮展.
목적 평개c-Jun안기말단격매(JNK)재대서내독소성급성폐손상중적작용.방법 웅성성년SD대서80지,체중250～300 g,채용수궤수자표법,장기수궤분위4조(n=20):대조조(C조)、급성폐손상조(ALI조)、SP600125조(S조)화이갑기아풍조(D조).ALI조、S조화D조미정맥주사LPS 5 mg/kg,C조미정맥주사등용량생리염수;S조화D조급여LPS후,분별미정맥주사JNK억제제SP600125 30 mg/kg혹이갑기아풍0.2 ml.우급여LPS후4 h시,각조처사10지대서,회수지기관폐포관세액(BALF)병취폐조직,채용ELISA법검측BALF중TNF-α화IL-1β적농도,계산폐조직습중/간중비(W/D비),관찰폐조직병이학결과,병진행폐손상평분.각조기여10지대서관찰지급여LPS후48 h,기록대서생존정황.결과 여C조비교,기여각조BALF중TNF-α화IL-1β적농도、폐조직W/D비화폐손상평분승고,생존솔강저(P<0.05혹0.01);여ALI조비교,S조BALF중TNF-α화IL-1도、폐조직W/D비화폐손상평분강저,생존솔승고(P<0.01),D조차이무통계학의의(P>0.05).결론 JNK적활화삼여료대서내독소성급성폐손상적발생발전.
Objective To evaluate the role of c-Jun N-terminal kinase (JNK) in lipopolysaccharide (LPS)-induced acute lung injury ( ALI) in rats.Methods Eighty male SD rats weighing 250-300 g were randomly divided into 4 groups ( n = 20 each) : control group (group C) ; ALI group; LPS + SP600125 (JNK inhibitor)group (group S) and LPS+ DMSO (the solvent) group (group DMSO) . ALI was induced by intravenous LPS 5mg/kg. In S and DMSO groups, SP600125 30 mg/kg and DMSO 0.2 ml were injected intravenously after LPS administration respectively. Ten animals were sacrificed by exsanguinafions at 4 h after LPS administration in each group. The broncho-alveolar lavage fluid (BALF) was colleted. The TNF-α and IL-1β concentrations in BALF were measured. The lungs were removed for microscopic examination and determination of W/D lung weight ratio. The other 10 animals in each group were observed for 48 h survival rate. Results Intravenous LPS significantly increased TNF-α and IL-1β concentrations in BALF and W/D lung weight ratio, decreased 48 h survival rate and induced histologic damage. Intravenous SP600125 30 mg/kg significantly attenuated the above-mentioned LPS-induced changes. Conclusion Activation of JNK is involved in the development of endotoxin-induced ALI in rats.
