中国医药导报
中國醫藥導報
중국의약도보
CHINA MEDICAL HERALD
2014年
17期
4-7,12
,共5页
袁绍鹏%白金叶%章菽%程桂芳%侯琦
袁紹鵬%白金葉%章菽%程桂芳%侯琦
원소붕%백금협%장숙%정계방%후기
人工麝香%哮喘%气道炎症%中性粒细胞%白介素17
人工麝香%哮喘%氣道炎癥%中性粒細胞%白介素17
인공사향%효천%기도염증%중성립세포%백개소17
Artifitial musk%Asthma%Airway inflamma-tion%Neutrophil%IL-17
目的:研究人工麝香对卵白蛋白(OVA)致敏引发的小鼠气道炎症损伤的保护作用及其机制。方法雄性Balb/c小鼠分别于第0天和第14天腹腔注射20μg OVA和2.25 mg Al(OH)3凝胶致敏,于第28、29、30天从气管滴入OVA进行攻击,攻击前1 h给予受试化合物人工麝香及阳性药地塞米松。小鼠随机分为6组院正常对照组(n=11)、模型组(OVA组,n=10)、地塞米松组(Dex组,n=10)、人工麝香给药10 d组(n=11)、人工麝香给药7 d组(n=13)、人工麝香给药5 d组(n=11)。人工麝香皮下给药100 mg/kg,分别自致敏第21、24、26天开始给药,给药周期为10、7、5 d。处死小鼠后,对小鼠的体重、脾脏和胸腺进行称重,计算脾脏、胸腺指数。检测支气管肺泡灌洗液(BALF)炎症细胞及炎症因子IL-4、IL-5及IL-17含量改变,HE染色分析小鼠肺部病理变化,免疫组化分析中性粒细胞生物标志物Ly6G/Gr-1的表达水平。结果与模型组相比,人工麝香100 mg/kg连续给药5、7 d可改善OVA致敏引发的小鼠气道炎症,明显降低小鼠BALF炎症细胞因子IL-4、IL-5、IL-17的含量(P<0.05)。细胞分类计数、肺组织病理分析及免疫组化结果表明,人工麝香能够抑制小鼠肺部气道中炎症细胞,特别是中性粒细胞的浸润,以及中性粒细胞标志物Ly6G/Gr-1的表达。结论人工麝香具有较强的减轻OVA致敏引发的小鼠气道炎症损伤的功能,提示人工麝香对于哮喘可能有一定的治疗作用。
目的:研究人工麝香對卵白蛋白(OVA)緻敏引髮的小鼠氣道炎癥損傷的保護作用及其機製。方法雄性Balb/c小鼠分彆于第0天和第14天腹腔註射20μg OVA和2.25 mg Al(OH)3凝膠緻敏,于第28、29、30天從氣管滴入OVA進行攻擊,攻擊前1 h給予受試化閤物人工麝香及暘性藥地塞米鬆。小鼠隨機分為6組院正常對照組(n=11)、模型組(OVA組,n=10)、地塞米鬆組(Dex組,n=10)、人工麝香給藥10 d組(n=11)、人工麝香給藥7 d組(n=13)、人工麝香給藥5 d組(n=11)。人工麝香皮下給藥100 mg/kg,分彆自緻敏第21、24、26天開始給藥,給藥週期為10、7、5 d。處死小鼠後,對小鼠的體重、脾髒和胸腺進行稱重,計算脾髒、胸腺指數。檢測支氣管肺泡灌洗液(BALF)炎癥細胞及炎癥因子IL-4、IL-5及IL-17含量改變,HE染色分析小鼠肺部病理變化,免疫組化分析中性粒細胞生物標誌物Ly6G/Gr-1的錶達水平。結果與模型組相比,人工麝香100 mg/kg連續給藥5、7 d可改善OVA緻敏引髮的小鼠氣道炎癥,明顯降低小鼠BALF炎癥細胞因子IL-4、IL-5、IL-17的含量(P<0.05)。細胞分類計數、肺組織病理分析及免疫組化結果錶明,人工麝香能夠抑製小鼠肺部氣道中炎癥細胞,特彆是中性粒細胞的浸潤,以及中性粒細胞標誌物Ly6G/Gr-1的錶達。結論人工麝香具有較彊的減輕OVA緻敏引髮的小鼠氣道炎癥損傷的功能,提示人工麝香對于哮喘可能有一定的治療作用。
목적:연구인공사향대란백단백(OVA)치민인발적소서기도염증손상적보호작용급기궤제。방법웅성Balb/c소서분별우제0천화제14천복강주사20μg OVA화2.25 mg Al(OH)3응효치민,우제28、29、30천종기관적입OVA진행공격,공격전1 h급여수시화합물인공사향급양성약지새미송。소서수궤분위6조원정상대조조(n=11)、모형조(OVA조,n=10)、지새미송조(Dex조,n=10)、인공사향급약10 d조(n=11)、인공사향급약7 d조(n=13)、인공사향급약5 d조(n=11)。인공사향피하급약100 mg/kg,분별자치민제21、24、26천개시급약,급약주기위10、7、5 d。처사소서후,대소서적체중、비장화흉선진행칭중,계산비장、흉선지수。검측지기관폐포관세액(BALF)염증세포급염증인자IL-4、IL-5급IL-17함량개변,HE염색분석소서폐부병리변화,면역조화분석중성립세포생물표지물Ly6G/Gr-1적표체수평。결과여모형조상비,인공사향100 mg/kg련속급약5、7 d가개선OVA치민인발적소서기도염증,명현강저소서BALF염증세포인자IL-4、IL-5、IL-17적함량(P<0.05)。세포분류계수、폐조직병리분석급면역조화결과표명,인공사향능구억제소서폐부기도중염증세포,특별시중성립세포적침윤,이급중성립세포표지물Ly6G/Gr-1적표체。결론인공사향구유교강적감경OVA치민인발적소서기도염증손상적공능,제시인공사향대우효천가능유일정적치료작용。
Objective To investigate the effects of artifitial musk on attenuation of OVA-challenged murine airway in-flammation in vivo and its mechanism. Methods Male Balb/c mice were divided into 6 groups, including control (n=11), OVA model (n=10), Dex (n=10), artifitial musk 10 days (n=11), artifitial musk 7 days (n=13), and artifitial musk 5 days (n=11). Mice were immunized intraperitoneally with 20 μg ovalbumin (OVA) and 4 mg Al (OH)3 suspended in 0.1 mL saline solution on Day 0 and Day 14, and then intratracheally challenged with 1% OVA suspended in saline solution on Days 28-30. Artifitial musk (100 mg/kg, s.c.) was given 1 hour before each OVA challenge for 5, 7 and 10 days since the sensitization for 21, 24, 26 days, respectively. After sacrificed, the body weights, spleen index and thymus in-dex were calculated. In addition, pathologic changes in the lung tissues, number of inflammatory cells in bronchoalveo-lar lavage fluid (BALF) and expression levels of IL-4, IL-5, IL-17 were observed. Moreover, the expression levels of Ly6G/Gr-1, a major biomarker of neutrophil, was detected by immunohistochemical examination. Results Compared with OVA model, the airway inflammation in mice improved after treatment with 100 mg/kg artifitial musk for 5 and 7 days in v iv o. Moreover, the expression levels of major cytokines as IL-4, IL-5 and IL-17 in BALF were inhibited after treatment with musk (P< 0.05). Pathological and cell count results showed that the inflammatory cell especially neu-trophile granulocyte infiltration in the airway section reduced after treatment with artifitial musk. Furthermore, immuno-histochemical examination results showed that the expression levels of Ly6G/Gr-1 were inhibited upon the treatment. Conclusion The results showed that artifitial musk pos-sesses inhibitory effects on airway inflammation induced with OVA in v iv o and the therapeutic function on asthma in the future.