国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2010年
23期
1417-1420
,共4页
应延风%李睿淳%毛宇飞%胡野%金耀建%屠平光
應延風%李睿淳%毛宇飛%鬍野%金耀建%屠平光
응연풍%리예순%모우비%호야%금요건%도평광
哮喘%前列腺素D2受体%嗜酸粒细胞
哮喘%前列腺素D2受體%嗜痠粒細胞
효천%전렬선소D2수체%기산립세포
Asthma%Prostaglandin D2 receptor%Eosinophil
目的 前列腺素D2(PGD2)通过嗜酸粒细胞(EOS)上前列腺素受体(DP1/CRTH2)调控其分化、成熟、迁移和募集功能,本研究试图了解在哮喘时外周血PGD2水平和EOS上DP1/CRTH2受体表达改变,探讨哮喘时EOS气道中浸润的机制.方法 20只雄性SD清洁级大鼠,随机分为正常对照组、哮喘组,每组10只.用卵白蛋白(OVA)雾化诱喘.用放射配体法分析其外周血EOS上的PGD2受体;用ELISA测定大鼠血中PG D2水平;肺组织病理切片,HE染色镜检.结果 与正常对照组相比,哮喘组大鼠支气管壁有显著的淋巴细胞和EOS浸润,具有典型的哮喘病变,哮喘组外周血PGD2水平显著高于正常对照组(P<0.01),哮喘组外周血和支气管肺泡灌洗液中EOS计数较正常对照组显著增加(P<0.01);哮喘组与正常对照组相比外周血EOS上DP总结合和CRTH2受体结合容量显著增加(P<0.01),DP1差异无统计学意义(P>0.05).结论 大鼠哮喘模型中外周血PGD2水平增高,同时EOS细胞上CRTH2受体表达增多,增高的PGD2可通过CRTH2信号转导途径,使EOS趋化作用增强,向气道内浸润,产生炎症效应,导致哮喘病理上EOS浸润特征.
目的 前列腺素D2(PGD2)通過嗜痠粒細胞(EOS)上前列腺素受體(DP1/CRTH2)調控其分化、成熟、遷移和募集功能,本研究試圖瞭解在哮喘時外週血PGD2水平和EOS上DP1/CRTH2受體錶達改變,探討哮喘時EOS氣道中浸潤的機製.方法 20隻雄性SD清潔級大鼠,隨機分為正常對照組、哮喘組,每組10隻.用卵白蛋白(OVA)霧化誘喘.用放射配體法分析其外週血EOS上的PGD2受體;用ELISA測定大鼠血中PG D2水平;肺組織病理切片,HE染色鏡檢.結果 與正常對照組相比,哮喘組大鼠支氣管壁有顯著的淋巴細胞和EOS浸潤,具有典型的哮喘病變,哮喘組外週血PGD2水平顯著高于正常對照組(P<0.01),哮喘組外週血和支氣管肺泡灌洗液中EOS計數較正常對照組顯著增加(P<0.01);哮喘組與正常對照組相比外週血EOS上DP總結閤和CRTH2受體結閤容量顯著增加(P<0.01),DP1差異無統計學意義(P>0.05).結論 大鼠哮喘模型中外週血PGD2水平增高,同時EOS細胞上CRTH2受體錶達增多,增高的PGD2可通過CRTH2信號轉導途徑,使EOS趨化作用增彊,嚮氣道內浸潤,產生炎癥效應,導緻哮喘病理上EOS浸潤特徵.
목적 전렬선소D2(PGD2)통과기산립세포(EOS)상전렬선소수체(DP1/CRTH2)조공기분화、성숙、천이화모집공능,본연구시도료해재효천시외주혈PGD2수평화EOS상DP1/CRTH2수체표체개변,탐토효천시EOS기도중침윤적궤제.방법 20지웅성SD청길급대서,수궤분위정상대조조、효천조,매조10지.용란백단백(OVA)무화유천.용방사배체법분석기외주혈EOS상적PGD2수체;용ELISA측정대서혈중PG D2수평;폐조직병리절편,HE염색경검.결과 여정상대조조상비,효천조대서지기관벽유현저적림파세포화EOS침윤,구유전형적효천병변,효천조외주혈PGD2수평현저고우정상대조조(P<0.01),효천조외주혈화지기관폐포관세액중EOS계수교정상대조조현저증가(P<0.01);효천조여정상대조조상비외주혈EOS상DP총결합화CRTH2수체결합용량현저증가(P<0.01),DP1차이무통계학의의(P>0.05).결론 대서효천모형중외주혈PGD2수평증고,동시EOS세포상CRTH2수체표체증다,증고적PGD2가통과CRTH2신호전도도경,사EOS추화작용증강,향기도내침윤,산생염증효응,도치효천병리상EOS침윤특정.
Objective Prostaglandin D2 (PGD2) has been shown to have regulating functions of the differentiation, maturation, migration and recruitment on eosinophils(EOS). This occurs through the interaction of PGD2 with the receptor expressed on EOS. This study attempts to understand the levels of prostaglandins and the change of DP1/CRTH2 receptors on EOS in asthma,to explore the mechanism of the infiltration of EOS in airway. Methods Twenty male SD rats were randomly divided into normal control group( n = 10), asthma group( n = 10). Asthma was induced by ovalbumin challenge. PGD2 receptor on EOS were measured by radiological binding assay. PGD2 levels in peripheral blood was measured by ELISA. The left lung was used for histological examinations and bronchalveolar lavage fluid (BALF) was collected from the right lung. Results Compared with the normal control group, asthma group had significant infiltration of EOS and lymphocytes in bronchial wall,there was the typical changes of asthma. PGD2 in peripheral blood in asthma group was significantly higher than the normal control group ( P < 0.01 =, EOS count in peripheral blood and BALF in normal control group increased significantly ( P <0.01 =. DP total binding capacity and CRTH2 binding capacity on EOS in asthma group were significantly higher than the control group ( P <0.01 =. DP1 was no significant differences ( P >0. 05). Conclusions PGD2 was significantly increased in asthma, and the CRTH2 receptor on EOS increased expression. The increased production of PGD2 EOS will strengthen the role of chemotaxis,infiltration to the airway,leading to arguments on EOS infiltration characteristics in asthma.