中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2008年
9期
952-955
,共4页
杨丽萍%张育才%汤定华%滕国良%张宇鸣
楊麗萍%張育纔%湯定華%滕國良%張宇鳴
양려평%장육재%탕정화%등국량%장우명
血管活性肠肽%内毒素休克%肺损伤%细胞因子%鼠
血管活性腸肽%內毒素休剋%肺損傷%細胞因子%鼠
혈관활성장태%내독소휴극%폐손상%세포인자%서
Vasoactive intestinal peptide%Endotoxic shock%Lung injury%Cytokines%Rat
目的 观察血管活性肠肽(VIP)对内毒索性休克大鼠肺损伤的作用,并探讨其可能机制.方法 SD大鼠静脉注射内毒素(E Coil LPS O111B4)10 mg/kg制作内毒素休克模型.随机将30只大鼠分成对照组(生理盐水,n=10)、内毒素组(内毒素10 mg/kg,n=10)和VIP组(内毒素10mg/kg+VIP 5 nmol,n=10).注药6 h后留取标本,测定各组肺干/湿比(W/D值)、支气管灌洗液(BALF)蛋白浓度和中性粒细胞计数,酶联免疫吸附法(ELISA)测定血清及BALF的肿瘤坏死因子-α(TNF-α)、白介紊-1(IL-1)和IL-10水平,观察肺组织病理变化(光镜+电镜).结果 内毒素组肺W/D值、BALF蛋白浓度和中性粒细胞计数比为(4.75±0.31),(68±6)%,(260±72)mg/L,对照组和VIP组分别为(3.61±0.28),(15±9)%,(70±21)mg/L和(4.02±0.25),(44±8)%,(123±44)mg/L,差异具有统计学意义(P＜0.05).内毒索组血清和BLAF中的TNF-α、IL-1β、IL-10明显升高(P＜0.05),VIP组与内毒素组比较TNF-α、IL-1β明显降低(P＜0.05),但仍高于对照组,IL-10较内毒素组进一步升高.光镜和电镜下VIP组病变轻于内毒素组.结论 VIP可减轻大鼠内毒索休克肺损伤,其作用机制可能与调控炎症细胞因子的表达有关.
目的 觀察血管活性腸肽(VIP)對內毒索性休剋大鼠肺損傷的作用,併探討其可能機製.方法 SD大鼠靜脈註射內毒素(E Coil LPS O111B4)10 mg/kg製作內毒素休剋模型.隨機將30隻大鼠分成對照組(生理鹽水,n=10)、內毒素組(內毒素10 mg/kg,n=10)和VIP組(內毒素10mg/kg+VIP 5 nmol,n=10).註藥6 h後留取標本,測定各組肺榦/濕比(W/D值)、支氣管灌洗液(BALF)蛋白濃度和中性粒細胞計數,酶聯免疫吸附法(ELISA)測定血清及BALF的腫瘤壞死因子-α(TNF-α)、白介紊-1(IL-1)和IL-10水平,觀察肺組織病理變化(光鏡+電鏡).結果 內毒素組肺W/D值、BALF蛋白濃度和中性粒細胞計數比為(4.75±0.31),(68±6)%,(260±72)mg/L,對照組和VIP組分彆為(3.61±0.28),(15±9)%,(70±21)mg/L和(4.02±0.25),(44±8)%,(123±44)mg/L,差異具有統計學意義(P＜0.05).內毒索組血清和BLAF中的TNF-α、IL-1β、IL-10明顯升高(P＜0.05),VIP組與內毒素組比較TNF-α、IL-1β明顯降低(P＜0.05),但仍高于對照組,IL-10較內毒素組進一步升高.光鏡和電鏡下VIP組病變輕于內毒素組.結論 VIP可減輕大鼠內毒索休剋肺損傷,其作用機製可能與調控炎癥細胞因子的錶達有關.
목적 관찰혈관활성장태(VIP)대내독색성휴극대서폐손상적작용,병탐토기가능궤제.방법 SD대서정맥주사내독소(E Coil LPS O111B4)10 mg/kg제작내독소휴극모형.수궤장30지대서분성대조조(생리염수,n=10)、내독소조(내독소10 mg/kg,n=10)화VIP조(내독소10mg/kg+VIP 5 nmol,n=10).주약6 h후류취표본,측정각조폐간/습비(W/D치)、지기관관세액(BALF)단백농도화중성립세포계수,매련면역흡부법(ELISA)측정혈청급BALF적종류배사인자-α(TNF-α)、백개문-1(IL-1)화IL-10수평,관찰폐조직병리변화(광경+전경).결과 내독소조폐W/D치、BALF단백농도화중성립세포계수비위(4.75±0.31),(68±6)%,(260±72)mg/L,대조조화VIP조분별위(3.61±0.28),(15±9)%,(70±21)mg/L화(4.02±0.25),(44±8)%,(123±44)mg/L,차이구유통계학의의(P＜0.05).내독색조혈청화BLAF중적TNF-α、IL-1β、IL-10명현승고(P＜0.05),VIP조여내독소조비교TNF-α、IL-1β명현강저(P＜0.05),단잉고우대조조,IL-10교내독소조진일보승고.광경화전경하VIP조병변경우내독소조.결론 VIP가감경대서내독색휴극폐손상,기작용궤제가능여조공염증세포인자적표체유관.
Objective To investigate the effects, and possible mechanism of action, of vasoactive intestinal peptide (VIP) on acute lung injury in a rodent model of endotoxic shock. Method Endotoxic shock was induced in Sprague-Dawley (SD) rats by intravenous injection of lipopolysacchaiide (LPS) at 10 mg/kg. Three groups (each group with 10 rats), were given injections of either normal saline (Control), LPS 10 mg/kg (LPS group), or LPS 10 mg/kg + VIP 5nmol (VIP). Samples were collected 6 hours after injection. Indices of lung injury including lung wet/dry weight ratio, protein concentration and neutrophil count in bronchoalveolar lavage fluid( BALF) were derived. Assays of TNF-α,IL-1β, IL-10 in serum and BALF were performed using ELISA. Light and electron microscopy were used to detect histopathological changes in lung tissues. Results The lung wet/dry weight ratio, protein concentration and neutrophil count in BALF were significantly raised in the LPS group compared to the Control group (P ＜ 0.05). These indices were significantly lowered in the VIP group compared to the LPS group, though not to the level of the control group. Concentrations of TNF-α, IL-1β, IL-10 in serum and BLAF also increased in the LPS group compared to the control group (P ＜ 0.0S). Levels of TNF-α and IL-1β were significantly lowered in the VTP group compared to the LPS group (P ＜ 0.05), while levels of IL-10 was significantly raised ( P ＜ 0.05). Histopathological changes due to lung injury were not as severe in the VIP group compared to the LPS group. CondusKms VIP plays a protective role during acute lung injury induced by endotoxic shock in rats. Its mechanism of action may be related to down-regulation of proinflammatory cytokines and up-regulation of anti inflammatory cytokines.
