中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2009年
2期
111-114
,共4页
吴妍雯%白明%张建初%金阳%张蕾%包滨
吳妍雯%白明%張建初%金暘%張蕾%包濱
오연문%백명%장건초%금양%장뢰%포빈
呼吸窘迫综合征,成人%环氧化酶2%Toll样受体4%一氧化氮%脂多糖类
呼吸窘迫綜閤徵,成人%環氧化酶2%Toll樣受體4%一氧化氮%脂多糖類
호흡군박종합정,성인%배양화매2%Toll양수체4%일양화담%지다당류
Respiratory distress syndrome,adult%Cyclooxygenase 2%Toll-like receptor 4%Nitric oxide%Lipopolysaccharides
目的 建立脂多糖致大鼠急性肺损伤的模型,观察一氧化氮对大鼠气道环氧合酶-2(cox-2)和Toll样受体4(TLR4)的分布及表达的影响.方法 健康雄性SD大鼠24只,按随机数字表法分为正常对照组、单用脂多糖(脂多糖组)、脂多糖加NO 20×10-6mg/L(低浓度NO组),脂多糖加NO 100×10-6mg/L(高浓度NO组).气管内滴注脂多糖(5 mg/kg)建立大鼠急性肺损伤模型.观察6 h后的肺水肿程度、免疫组织化学(SP染色)和实时荧光定量PCR检测肺组织中COX-2和TLR4的表达,以及分别吸入20×10-6、100×10-6mg/L浓度NO后的影响.所得数据采用单因素方差分析进行统计学分析,多个样本均数之间的两两比较采用LSD-t检验.结果 COX-2和TLR4在对照组大鼠气道内有广泛的分布和表达.脂多糖组大鼠肺水肿程度明显高于对照组,其主支气管和肺内细支气管上皮细胞内COX-2(6.5±2.8)及TLR4(44.9±11.3)表达高于对照组(分别为2.8 4±0.8、2.1±0.7),差异有统计学意义(t值分别为3.003、10.480,均P<0.01).低浓度NO组肺水肿程度明显减轻,其COX-2表达量(5.0±2.0)低于脂多糖组,但差异无统计学意义(t=1.227,P>0.05).而低浓度NO组TLR4(16.2±3.8)的表达量与脂多糖组(44.9±11.3)比较差异具有统计学意义(t=7.030,P<0.001).结论 COX-2和TLR4在大鼠气道内广泛分布,脂多糖刺激可使COX-2和TLR4的表达增强,吸入适当浓度NO可降低由脂多糖引起的COX-2和TLR4表达的增高.
目的 建立脂多糖緻大鼠急性肺損傷的模型,觀察一氧化氮對大鼠氣道環氧閤酶-2(cox-2)和Toll樣受體4(TLR4)的分佈及錶達的影響.方法 健康雄性SD大鼠24隻,按隨機數字錶法分為正常對照組、單用脂多糖(脂多糖組)、脂多糖加NO 20×10-6mg/L(低濃度NO組),脂多糖加NO 100×10-6mg/L(高濃度NO組).氣管內滴註脂多糖(5 mg/kg)建立大鼠急性肺損傷模型.觀察6 h後的肺水腫程度、免疫組織化學(SP染色)和實時熒光定量PCR檢測肺組織中COX-2和TLR4的錶達,以及分彆吸入20×10-6、100×10-6mg/L濃度NO後的影響.所得數據採用單因素方差分析進行統計學分析,多箇樣本均數之間的兩兩比較採用LSD-t檢驗.結果 COX-2和TLR4在對照組大鼠氣道內有廣汎的分佈和錶達.脂多糖組大鼠肺水腫程度明顯高于對照組,其主支氣管和肺內細支氣管上皮細胞內COX-2(6.5±2.8)及TLR4(44.9±11.3)錶達高于對照組(分彆為2.8 4±0.8、2.1±0.7),差異有統計學意義(t值分彆為3.003、10.480,均P<0.01).低濃度NO組肺水腫程度明顯減輕,其COX-2錶達量(5.0±2.0)低于脂多糖組,但差異無統計學意義(t=1.227,P>0.05).而低濃度NO組TLR4(16.2±3.8)的錶達量與脂多糖組(44.9±11.3)比較差異具有統計學意義(t=7.030,P<0.001).結論 COX-2和TLR4在大鼠氣道內廣汎分佈,脂多糖刺激可使COX-2和TLR4的錶達增彊,吸入適噹濃度NO可降低由脂多糖引起的COX-2和TLR4錶達的增高.
목적 건립지다당치대서급성폐손상적모형,관찰일양화담대대서기도배양합매-2(cox-2)화Toll양수체4(TLR4)적분포급표체적영향.방법 건강웅성SD대서24지,안수궤수자표법분위정상대조조、단용지다당(지다당조)、지다당가NO 20×10-6mg/L(저농도NO조),지다당가NO 100×10-6mg/L(고농도NO조).기관내적주지다당(5 mg/kg)건립대서급성폐손상모형.관찰6 h후적폐수종정도、면역조직화학(SP염색)화실시형광정량PCR검측폐조직중COX-2화TLR4적표체,이급분별흡입20×10-6、100×10-6mg/L농도NO후적영향.소득수거채용단인소방차분석진행통계학분석,다개양본균수지간적량량비교채용LSD-t검험.결과 COX-2화TLR4재대조조대서기도내유엄범적분포화표체.지다당조대서폐수종정도명현고우대조조,기주지기관화폐내세지기관상피세포내COX-2(6.5±2.8)급TLR4(44.9±11.3)표체고우대조조(분별위2.8 4±0.8、2.1±0.7),차이유통계학의의(t치분별위3.003、10.480,균P<0.01).저농도NO조폐수종정도명현감경,기COX-2표체량(5.0±2.0)저우지다당조,단차이무통계학의의(t=1.227,P>0.05).이저농도NO조TLR4(16.2±3.8)적표체량여지다당조(44.9±11.3)비교차이구유통계학의의(t=7.030,P<0.001).결론 COX-2화TLR4재대서기도내엄범분포,지다당자격가사COX-2화TLR4적표체증강,흡입괄당농도NO가강저유지다당인기적COX-2화TLR4표체적증고.
Objective To study the effect of nitric oxide (NO) on the expression of cyclo-oxgenase 2 ( COX-2) and toll-like receptor 4 ( TLR4) in a rat model of acute lung injury ( ALI) induced by lipopolysaccharide ( LPS). Methods Twenty-four Sprague-Dawley rats were randomly divided into 4 groups. Group N: normal control group; Group L: ALI model by LPS intratracheal instillation; Group Za: ALI model + inhaled NO 20 × 10-6 mg/L; Group Zb: ALI model + inhaled NO 100 × 10-6 mg/L. Lung morphology was studied and COX-2 was detected by immunohistochemistry (IHC) while TLR4 by fluorescent quantitative PCR( FQ-PCR) . Results Immunohistochemistry and FQ-PCR showed that COX-2(2. 8 ± 0. 8 ) and TLR4(2. 1 ±0.7) were detected in the respiratory tract of the normal control rats. In Group L, the expression of COX-2 ( 6. 5 ±2.8) and TLR4(44. 9 ± 11.3) was increased in the main bronchus and bronchioles, compared to the normal controls (t =3.003, 10.480, both P < 0. 01). In Group Zb, the expression of COX-2(5. 0 ±2. 0) and TLR4( 16. 2 ±3. 8) were decreased as compared to Group L, but only the level of TI.R4 showed statistical difference (t = 7. 030,P < 0. 001 ). Conclusions COX-2 and TLR4 distributed widely in the respiratory tract of the rats. LPS increased the expression of COX-2 and TLR4. Low dose of nitric oxide(20 × 10-6 mg/L) inhalation reduced the bronchiolar expression of COX-2 and TLR4 induced by LPS.
