雷公藤甲素对哮喘小鼠白介素13和嗜酸性粒细胞趋化因子表达的影响

目的观察雷公藤甲素(TL)对哮喘小鼠肺组织中白介素13(IL-13)和嗜酸性粒细胞趋化因子(Eotaxin)表达的影响,探讨TL治疗哮喘的作用机理。方法40只雄性昆明小鼠随机分成4组:正常对照组、哮喘未治疗组、地塞米松治疗组及TL治疗组,以卵清蛋白致敏和激发方法建立哮喘小鼠动物模型并给予相应治疗。24 d后处死小鼠,检测各组支气管肺泡灌洗液(BALF)中白细胞总数及嗜酸性粒细胞(Eos)计数;采用逆转录-聚合酶链反应(RT-PCR)方法检测各组小鼠肺组织匀浆中IL-13、eotaxin mRNA的表达量;采用免疫组化法检测各组小鼠肺组织切片中IL-13、eotaxin蛋白的表达水平;并探讨他们之间的关系。结果哮喘未治疗组小鼠肺组织IL-13、eotaxin mRNA及蛋白的表达量均明显高于正常对照组(P<0.01),TL治疗组及地塞米松治疗组低于哮喘未治疗组(P<0.01或<0.05)。肺组织IL-13蛋白的表达与BALF中的白细胞总数、Eos计数及肺组织eotaxin蛋白的表达呈正相关(r分别为0.513、0.604、0.625,P<0.01)。肺组织eotaxin蛋白的表达与BALF中的白细胞总数、Eos计数呈正相关(r分别为0.679、0.718,P<0.01)。结论TL抑制哮喘气道炎症的机制可能与其抑制肺组织中IL-13及eotaxin的表达有关。     

Peridinin from the Marine Symbiotic Dinoflagellate,Symbiodinium sp., Regulates Eosinophilia in Mice

Peridinin and fucoxanthin, which are natural carotenoids isolated from a symbiotic dinoflagellate, Symbiodinium sp., and a brown alga, Petalonia fascia, respectively, were compared for inhibitory effects on delayed-type hypersensitivity in mice. The number of eosinophils at the site of inflammation and in peripheral blood was compared for the administration of peridinin and fucoxanthin applied by painting and intraperitoneally. Peridinin, but not the structurally-related fucoxanthin, significantly suppressed the number of eosinophils in both the ear lobe and peripheral blood. Furthermore, peridinin applied topically, but not administered intraperitoneally, suppressed the level of eotaxin in the ears of sensitized mice. Fucoxanthin weakly suppressed the concentration of eotaxin in ears only by intraperitoneal administration. Although both carotenoids inhibited the migration of eosinophils toward eotaxin, the inhibitory effect of peridinin was higher than that of fucoxanthin. Peridinin may be a potential agent for suppressing allergic inflammatory responses, such as atopic dermatitis, in which eosinophils play a major role in the increase of inflammation.     

班布特罗对哮喘豚鼠气道嗜酸性粒细胞炎症的作用机理研究

卵白蛋白致敏(OA)建立豚鼠哮喘模型,用不同剂量的班布特罗(Bam)灌胃,密度梯度离心法分离支气管肺泡灌洗液(BALF)中低密度嗜酸性粒细胞(HEos)和正常密度嗜酸性粒细胞(NEos),原位末端标记法(TUNEL)检测嗜酸性粒细胞(Eos)凋亡,酶联免疫吸附(ELISA)法测定BALF中嗜酸性粒细胞趋化因子(Eotaxin)水平。结果表明:15、30mg·kg-1Bam可明显降低BALF中Eos数量和Eotaxin水平,但对Eos凋亡无影响。β-受体阻断剂普萘洛尔可阻断其作用,说明一定剂量的Bam可能通过抑制Eotaxin对Eos的选择性趋化作用降低BALF中Eos的数量,从而发挥对气道炎症的拮抗作用。