CAJ | 학술논문

目的探讨内毒素预处理对肝脏缺血-再灌注后肺损伤的影响及机制.方法将48只新西兰大白兔随机分为一般对照组(C一般组)和预处理对照组(C预处理组),缺血-再灌注组(IR组)和预处理再灌注组(LPS+IR组),每组12只.C一般组仅行手术解剖;C预处理组手术解剖前3 d分别经腹腔注射0.5、0.5和1.0 mg/kg脂多糖(LPS)进行内毒素预处理;IR组夹闭肝门30 rmn,再灌注4 h,进行肝脏缺血.再灌注;LPS+IR组行内毒素预处理后再行肝脏缺血.再灌注.检测各组再灌注后4 h血清内毒素、肿瘤坏死因子-α(TNF-α)、肺湿干比、灌洗液蛋白含量、组织匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)、肺损伤率及肺泡巨噬细胞核因子-KB(NF-kB)活性的变化.组间比较采用单因数方差分析.结果 C一般组和C预处理组各项检测指标差异无统计学意义(P>0.05).LPS+IR组血清TNF-α[(48.31±5.31)pg/ml vs.(56.47±5.09)pg/ml,P<0.01]、肺湿干比[(4.98±0.33)vs.(5.22±0.31),P=0.03]、灌洗液蛋白含量[(0.68±0.11)g/L vs.(0.76±0.10)g/L,P:0.04]、MDA[(0.86±0.06)mnol/mg vs.(0.93±0.07)nmoL/mg,P=0.02]、肺损伤率[(13.4±4.3)%vs.(17.4±4.1)%,P=0.03]及肺泡巨噬细胞NF-kB活性[(5.82±1.12)OD/m2 vs.(7.40±1.26)OD/mm2,P<0.01]明显低于IR组;同时LPS+IR组SOD[(90.30±7.38)U/mg vs.(84.44±7.90)U/mg,P=0.04]明显高于IR组.结论内毒素预处理可以减轻肝脏缺血.再灌注后肺损伤,其机制与降低了血清TNF-α产生及抑制肺泡巨噬细胞中NF-kB活化有关.
목적 탐토내독소예처리대간장결혈-재관주후폐손상적영향급궤제.방법 장48지신서란대백토수궤분위일반대조조(C일반조)화예처리대조조(C예처리조),결혈-재관주조(IR조)화예처리재관주조(LPS+IR조),매조12지.C일반조부행수술해부;C예처리조수술해부전3 d분별경복강주사0.5、0.5화1.0 mg/kg지다당(LPS)진행내독소예처리;IR조협폐간문30 rmn,재관주4 h,진행간장결혈.재관주;LPS+IR조행내독소예처리후재행간장결혈.재관주.검측각조재관주후4 h혈청내독소、종류배사인자-α(TNF-α)、폐습간비、관세액단백함량、조직균장병이철(MDA)、초양화물기화매(SOD)、폐손상솔급폐포거서세포핵인자-KB(NF-kB)활성적변화.조간비교채용단인수방차분석.결과 C일반조화C예처리조각항검측지표차이무통계학의의(P>0.05).LPS+IR조혈청TNF-α[(48.31±5.31)pg/ml vs.(56.47±5.09)pg/ml,P<0.01]、폐습간비[(4.98±0.33)vs.(5.22±0.31),P=0.03]、관세액단백함량[(0.68±0.11)g/L vs.(0.76±0.10)g/L,P:0.04]、MDA[(0.86±0.06)mnol/mg vs.(0.93±0.07)nmoL/mg,P=0.02]、폐손상솔[(13.4±4.3)%vs.(17.4±4.1)%,P=0.03]급폐포거서세포NF-kB활성[(5.82±1.12)OD/m2 vs.(7.40±1.26)OD/mm2,P<0.01]명현저우IR조;동시LPS+IR조SOD[(90.30±7.38)U/mg vs.(84.44±7.90)U/mg,P=0.04]명현고우IR조.결론 내독소예처리가이감경간장결혈.재관주후폐손상,기궤제여강저료혈청TNF-α산생급억제폐포거서세포중NF-kB활화유관.
Objective To investite the effect of endotoxin pretreatment on lung injury induced by hepatic ischemia reperfusion in rabbits and its mechanism. Method Forty-eight New Zealand white rabbits were randomly divided into4 groups with 12 rabbits each group:routine control group,pretreatment control group,ischemia reperfusion group (IR group), and preperfusion group( LPS + IR group). Rabbits of routine control group received operative dissector only, and those of pretreatment control group received pretratment of daily intraabdominal injection of lipopo|ysaccharide(O.5,0.5,and 1.0 mg/kg,respectively)in the 3 days before operative dissector.Livers of IR group were rendered and ischeraic for 30 minutes, and repeffused for up to 4 hours. Rabbits of LPS +IR group received the preueaunent before heretic ischemia repeffusion. Four hours after reperfusion, serum endotoxin,tumor necrosis factor-α(TNF-α), wet/dry ratio and broncho-alveolar lavage fluid protein content of lung,malondialdehyde(MDA) and mpenrxide dismutase(SOD) in lung homogenate, lung injury ratio, and activity of Nuclear factor-kB(NF-kB) in alveolar macrophage wene examined. Differences within the groups were analyzed using One way ANOVA. Results Between the two control groups,there were no significant differences in all indexes(P>0.05). The TNF-α[ (48.31±5.31)pg/ml vs.(56.47±5.09)pg/ml, P<0.01],wet/dry ratio [(4.98±0.33)vs. (5.22±0.31), P = 0.03],broncho-alveolar hvage fluid protein content[(0.68±0.11)g/L vs. (0.76±0.10)g/L, P =0.04],MDA[(0.86±0.06)nmol/mg vs. (0.93±0.07)nmol/mg, P =0.02],lung injury ra-tio[(13.4±4.3)% vs. (17.4±4.1)%, P = 0.03],and the activity of NF-gB[(5.82±1.12)OD/mm2 vs.(7.40±1.26)OD/mm2, P<0.01] in alveolar macrophage of the LPS+ IB group were all significantly lower than those of IB group, while the SOD[ (90.30±7.38 )U/rag vs. (84.44±7.90 )U/rag, P = 0.04]of LPS + IR group was significantly higher than that of IR group. Conclusions Endotoxin pretrealment may ameliorate the lung injury induced by hepatic isehernia reperfusion. The mechanism may be that endotoxin pretreatment deoreases production of serum TNF-α and the activity of NF-kB in alveolar maerophage.