湖南师范大学学报（医学版）
湖南師範大學學報（醫學版）
호남사범대학학보（의학판）
JOURNAL OF HUNAN NORMAL UNIVERSITY(MEDICAL SCIENCE)
2013年
2期
1-4,10
,共5页
臭氧%应激%气道高反应性
臭氧%應激%氣道高反應性
취양%응격%기도고반응성
ozone%stress%airway hyperresponsiveness
目的：初步探讨臭氧应激建立气道高反应（AHR）大鼠模型的机制。方法：20只SD大鼠随机分为正常对照组和臭氧应激组，每组10只。通过呼气相气道阻力（Re），支气管肺泡灌洗液（BALF）总蛋白、细胞计数、分类，肺组织病理切片等指标确定AHR大鼠模型建立的可靠性；同时测定血浆IgE水平，外周血单个核细胞（PBMC）培养后取上清物测定IFN-γ、IL-13，对O3应激引发AHR的机理进行初步探讨。结果：臭氧应激组与正常对照组比较，气道反应性，BLAF中细胞计数、分类，血浆IgE水平等各项指标均升高；肺组织病理切片存在明显的炎性细胞浸润；PBMC培养上清中IFN-γ、IL-13臭氧应激组明显升高。结论：外源性损伤因子O3攻击支气管上皮细胞，气道上皮细胞功能缺陷或失稳态，引发气道高反应，其机制可能与Th1及Th2类免疫反应同时激活嗜酸性粒细胞（EOS）炎症反应有关。
目的：初步探討臭氧應激建立氣道高反應（AHR）大鼠模型的機製。方法：20隻SD大鼠隨機分為正常對照組和臭氧應激組，每組10隻。通過呼氣相氣道阻力（Re），支氣管肺泡灌洗液（BALF）總蛋白、細胞計數、分類，肺組織病理切片等指標確定AHR大鼠模型建立的可靠性；同時測定血漿IgE水平，外週血單箇覈細胞（PBMC）培養後取上清物測定IFN-γ、IL-13，對O3應激引髮AHR的機理進行初步探討。結果：臭氧應激組與正常對照組比較，氣道反應性，BLAF中細胞計數、分類，血漿IgE水平等各項指標均升高；肺組織病理切片存在明顯的炎性細胞浸潤；PBMC培養上清中IFN-γ、IL-13臭氧應激組明顯升高。結論：外源性損傷因子O3攻擊支氣管上皮細胞，氣道上皮細胞功能缺陷或失穩態，引髮氣道高反應，其機製可能與Th1及Th2類免疫反應同時激活嗜痠性粒細胞（EOS）炎癥反應有關。
목적：초보탐토취양응격건립기도고반응（AHR）대서모형적궤제。방법：20지SD대서수궤분위정상대조조화취양응격조，매조10지。통과호기상기도조력（Re），지기관폐포관세액（BALF）총단백、세포계수、분류，폐조직병리절편등지표학정AHR대서모형건립적가고성；동시측정혈장IgE수평，외주혈단개핵세포（PBMC）배양후취상청물측정IFN-γ、IL-13，대O3응격인발AHR적궤리진행초보탐토。결과：취양응격조여정상대조조비교，기도반응성，BLAF중세포계수、분류，혈장IgE수평등각항지표균승고；폐조직병리절편존재명현적염성세포침윤；PBMC배양상청중IFN-γ、IL-13취양응격조명현승고。결론：외원성손상인자O3공격지기관상피세포，기도상피세포공능결함혹실은태，인발기도고반응，기궤제가능여Th1급Th2류면역반응동시격활기산성립세포（EOS）염증반응유관。
Objective To investigate the mechanisms to establish airway hyperresponsiveness (AHR) rat model by ozone stress. Methods 20 SD rats were randomly divided into normal control group and ozone group (n=10). Indicators including resistance of expiratory airway (Re), total protein in bronchoalveolar lavage fluid (BALF), cell count、classification, lung tissue biopsy to confirm the reliability of AHR rat model;detecting the IgE level in the serum simultaneously:after peripheral blood mononujclear cells (PBMC) culture, adopting the super-natant to detect the IFN-γ,IL-13, the mechanism that caused the AHR was primarily discussed. Results Com-paring the ozone group with normal control group, all of the indicators, including airway responsiveness,cell count and classification in the BLAF and IgE level in the serum elevated; lung biopsy showed obvious inflammatory cell infiltration;For the ozone group, IFN-γ、IL-13 in supernatant of PBMC culture elevated evidently compared with the normal control group. Conclusion After xogenous damage factor O3 attacked the bronchial epithelial cells, the airway epithelial cells function defected and homeostasis lost, causing airway hyperresponsiveness, whose mechanism may be related to eosinophils (EOS) inflammation activated by Th1 and Th2 type immune re-sponses simultaneously.
