中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2008年
6期
610-613
,共4页
张晓隆%王方岩%徐正祄%王万铁%郝卯林
張曉隆%王方巖%徐正祄%王萬鐵%郝卯林
장효륭%왕방암%서정개%왕만철%학묘림
红花注射液%肺%缺血再灌注损伤%超微结构%细胞间黏附分子-1
紅花註射液%肺%缺血再灌註損傷%超微結構%細胞間黏附分子-1
홍화주사액%폐%결혈재관주손상%초미결구%세포간점부분자-1
Safflor injection%Lung%Ischemia-reperfusion injury%Ultrastructure%Intercellular adhesion molecule-1
目的 探讨红花对兔肺缺血-再灌注损伤时细胞间黏附分子-1(ICAM-1)表达的影响及其机制.方法 复制在体兔单肺原位缺血-再灌注损伤模型.日本大耳兔30只,由温州医学院实验动物中心提供,随机分为3组(每组10只):假手术对照组(S组),缺血-再灌注组(I/R组)和缺血-再灌注+红花注射液组(SI组).SI组分别在缺血前20min和再灌注即刻静脉注射红花注射液(2.0mL/kg),实验结束时,自颈动脉抽血检测丙二醛(MDA)含量、超氧化物歧化酶(SOD)和黄嘌呤氧化酶(XO)活力;取肺组织测湿干重I:L(W/D),髓过氧化物酶(MPO)活力;电镜观察肺组织超微结构改变;免疫组化法检测肺组织ICAM-1蛋白表达.统计学处理采用单因素方差分析.结果 I/R组血清MDA、XO均显著高于S组(P<0.01),SOD明显低于S组(P<0.01);I/R组和sI组的W/D与MPO均高于S组(P<0.05或P<0.01),但SI组显著低于I/R组(P<0.01);I/R组肺组织的超微结构损伤严重,SI组损伤程度明显较轻;免疫组化发现I/R组肺组织ICAM-1(2.94±0.48)蛋白表达显著高于SI(1.75±0.62)组(P<0.01).结论 红花可通过下调ICAM-1蛋白的表达,抑制中性粒细胞聚集,降低氧自由基水平,减轻脂质过氧化反应,从而减轻肺缺血-再灌注损伤.
目的 探討紅花對兔肺缺血-再灌註損傷時細胞間黏附分子-1(ICAM-1)錶達的影響及其機製.方法 複製在體兔單肺原位缺血-再灌註損傷模型.日本大耳兔30隻,由溫州醫學院實驗動物中心提供,隨機分為3組(每組10隻):假手術對照組(S組),缺血-再灌註組(I/R組)和缺血-再灌註+紅花註射液組(SI組).SI組分彆在缺血前20min和再灌註即刻靜脈註射紅花註射液(2.0mL/kg),實驗結束時,自頸動脈抽血檢測丙二醛(MDA)含量、超氧化物歧化酶(SOD)和黃嘌呤氧化酶(XO)活力;取肺組織測濕榦重I:L(W/D),髓過氧化物酶(MPO)活力;電鏡觀察肺組織超微結構改變;免疫組化法檢測肺組織ICAM-1蛋白錶達.統計學處理採用單因素方差分析.結果 I/R組血清MDA、XO均顯著高于S組(P<0.01),SOD明顯低于S組(P<0.01);I/R組和sI組的W/D與MPO均高于S組(P<0.05或P<0.01),但SI組顯著低于I/R組(P<0.01);I/R組肺組織的超微結構損傷嚴重,SI組損傷程度明顯較輕;免疫組化髮現I/R組肺組織ICAM-1(2.94±0.48)蛋白錶達顯著高于SI(1.75±0.62)組(P<0.01).結論 紅花可通過下調ICAM-1蛋白的錶達,抑製中性粒細胞聚集,降低氧自由基水平,減輕脂質過氧化反應,從而減輕肺缺血-再灌註損傷.
목적 탐토홍화대토폐결혈-재관주손상시세포간점부분자-1(ICAM-1)표체적영향급기궤제.방법 복제재체토단폐원위결혈-재관주손상모형.일본대이토30지,유온주의학원실험동물중심제공,수궤분위3조(매조10지):가수술대조조(S조),결혈-재관주조(I/R조)화결혈-재관주+홍화주사액조(SI조).SI조분별재결혈전20min화재관주즉각정맥주사홍화주사액(2.0mL/kg),실험결속시,자경동맥추혈검측병이철(MDA)함량、초양화물기화매(SOD)화황표령양화매(XO)활력;취폐조직측습간중I:L(W/D),수과양화물매(MPO)활력;전경관찰폐조직초미결구개변;면역조화법검측폐조직ICAM-1단백표체.통계학처리채용단인소방차분석.결과 I/R조혈청MDA、XO균현저고우S조(P<0.01),SOD명현저우S조(P<0.01);I/R조화sI조적W/D여MPO균고우S조(P<0.05혹P<0.01),단SI조현저저우I/R조(P<0.01);I/R조폐조직적초미결구손상엄중,SI조손상정도명현교경;면역조화발현I/R조폐조직ICAM-1(2.94±0.48)단백표체현저고우SI(1.75±0.62)조(P<0.01).결론 홍화가통과하조ICAM-1단백적표체,억제중성립세포취집,강저양자유기수평,감경지질과양화반응,종이감경폐결혈-재관주손상.
Objective To investigate the influence of injection carthamus tinctorius D. (1C) on the expression of intercellular adhesion molecule-1(ICAM-1) during the ischemia-reperfusion injury of lung (LIRI) in rabbits and its potential mechanism. Method Single lung ischemia-reperfusion animal model was induced in rabbits. A total of 30 Japanese white rabbits were randomly divided into sham-operation group (S group, n =10), ischemia-reperfusion group (I/R group, re = 10) and ischemia-reperfusion plus 1C group (1C group, n = 10) .The rabbits of 1C group received 1C 2.0 ml/kg injected intravenously just at 20 min before ligation of artery involved and the same dose of 1C instantly at the initiation of reperfusion. Malondialdehyde (MDA) , superoxide dismutase (SOD) and xanthine oxidase(XO) in serum were measured. The lung tissue was sampled and assayed wet/dry weight ratio (W/D), contents of myeloperoxidase (MPO) at the end of the experiment, and ultrastructure changes were observed under electron microscope. The expression of ICAM-1 was measured by using immunohistochemistry(IHC) . snd one-way ANOVA was used for statistical analysis. Results In I/R group, serum XO and MDA increased and SOD decreased, whereas the same pattern of changes but less magnitude happened in 1C group ( P < 0.01). The values of W/D and MPO were much higher in I/R group, but lower in 1C group. Under electron microscope, the ultrastructure of lung tissue showed pathological changes in the rabbits of I/R group,and these changes were greatly attenuated in the rabbits of 1C group . The IHC showed that ICAM - 1 in lung tissue of I / R group was (2.94±0.48) which was significantly higher than that of 1C group(1.75 (P < 0.01). Conclusions Injection Carthamus tinctorius D. may meliorate the ischemia-reperfusion injury of lung by way of suppressing the expression of ICAM-1, inhibiting neutrophil aggregation, lowering oxygen free radical level and decreasing lipid peroxidation.
