中国医学装备
中國醫學裝備
중국의학장비
CHINA MEDICAL EQUIPMENT
2012年
3期
4-8
,共5页
姚秀娟%李艳%吕喆%袁慧慧%贾军会%赵文明%安云庆%王炜%黄克武%孙英
姚秀娟%李豔%呂喆%袁慧慧%賈軍會%趙文明%安雲慶%王煒%黃剋武%孫英
요수연%리염%려철%원혜혜%가군회%조문명%안운경%왕위%황극무%손영
过敏原%哮喘模型%急性期%亚急性期
過敏原%哮喘模型%急性期%亞急性期
과민원%효천모형%급성기%아급성기
Allergen%Asthma model%Acute phase%Sub-acute phase
目的:评估不同剂量过敏原对滴鼻制备小鼠急性和亚急性哮喘模型的影响。方法:将不同剂量卵清蛋白(OVA)25μg、50μg、100μg连续滴鼻,建立急性和亚急性小鼠哮喘模型。使用有创小鼠肺功能仪测量各组小鼠肺功能参数;收集小鼠肺泡灌洗液计数细胞总数和细胞分类;取其肺组织常规石蜡包埋切片,进行伊红染色(HE)、刚果红染色、马松染色和过碘酸雪夫氏(PAS)染色,观察炎性细胞浸润,胶原纤维沉积、黏液分泌等指标的变化。结果:在实验第20d和24d,100μg与50μgOVA激发组小鼠气道反应性、肺泡灌洗液中细胞总数和嗜酸性粒细胞百分比增高;小鼠肺泡、管腔、管壁及伴行动脉周围有大量炎性细胞特别是嗜酸性粒细胞浸润,支气管粘膜皱襞增多、延长,管腔内存有大量黏液性痰栓;支气管管壁及其伴行动脉周围胶原纤维沉积明显增加;气道粘蛋白染色成强阳性反应,较25μgOVA激发组和生理盐水组小鼠有明显差异。结论:采用不同剂量OVA滴鼻,成功建立了程度不同的急性和亚急性小鼠支气管哮喘模型。过敏原剂量对模型建立有重要影响,为进一步研究哮喘的发生机制和药物筛选奠定了基础。
目的:評估不同劑量過敏原對滴鼻製備小鼠急性和亞急性哮喘模型的影響。方法:將不同劑量卵清蛋白(OVA)25μg、50μg、100μg連續滴鼻,建立急性和亞急性小鼠哮喘模型。使用有創小鼠肺功能儀測量各組小鼠肺功能參數;收集小鼠肺泡灌洗液計數細胞總數和細胞分類;取其肺組織常規石蠟包埋切片,進行伊紅染色(HE)、剛果紅染色、馬鬆染色和過碘痠雪伕氏(PAS)染色,觀察炎性細胞浸潤,膠原纖維沉積、黏液分泌等指標的變化。結果:在實驗第20d和24d,100μg與50μgOVA激髮組小鼠氣道反應性、肺泡灌洗液中細胞總數和嗜痠性粒細胞百分比增高;小鼠肺泡、管腔、管壁及伴行動脈週圍有大量炎性細胞特彆是嗜痠性粒細胞浸潤,支氣管粘膜皺襞增多、延長,管腔內存有大量黏液性痰栓;支氣管管壁及其伴行動脈週圍膠原纖維沉積明顯增加;氣道粘蛋白染色成彊暘性反應,較25μgOVA激髮組和生理鹽水組小鼠有明顯差異。結論:採用不同劑量OVA滴鼻,成功建立瞭程度不同的急性和亞急性小鼠支氣管哮喘模型。過敏原劑量對模型建立有重要影響,為進一步研究哮喘的髮生機製和藥物篩選奠定瞭基礎。
목적:평고불동제량과민원대적비제비소서급성화아급성효천모형적영향。방법:장불동제량란청단백(OVA)25μg、50μg、100μg련속적비,건립급성화아급성소서효천모형。사용유창소서폐공능의측량각조소서폐공능삼수;수집소서폐포관세액계수세포총수화세포분류;취기폐조직상규석사포매절편,진행이홍염색(HE)、강과홍염색、마송염색화과전산설부씨(PAS)염색,관찰염성세포침윤,효원섬유침적、점액분비등지표적변화。결과:재실험제20d화24d,100μg여50μgOVA격발조소서기도반응성、폐포관세액중세포총수화기산성립세포백분비증고;소서폐포、관강、관벽급반행동맥주위유대량염성세포특별시기산성립세포침윤,지기관점막추벽증다、연장,관강내존유대량점액성담전;지기관관벽급기반행동맥주위효원섬유침적명현증가;기도점단백염색성강양성반응,교25μgOVA격발조화생리염수조소서유명현차이。결론:채용불동제량OVA적비,성공건립료정도불동적급성화아급성소서지기관효천모형。과민원제량대모형건립유중요영향,위진일보연구효천적발생궤제화약물사선전정료기출。
Objective: To evaluate effects of different doses of allergen on ovalbumin (OVA)-induced acute and sub-acute mouse models of asthma by intranasal challenge. Methods: In brief, intranasal inhalation challenge with different doses of OVA (25, 50 and 100μg, respectively) was performed to induce acute and sub-acute mouse models of asthma. The respiratory function parameters of excited group and control group were measured using an invasive pulmonary function device. After collecting bronchoalveolar lavage fluid (BALF) of each group the cells were counted. Histological staining with HE, Congo red, Masson and Periodic acid-Schiff (PAS) were employed in paraffin-embedded sections derived from the left lungs to identify inflammatory cell infiltration, collagen deposition, mucus expression and other indicators. Results: Compared with 25 μg OVA- challenged group and saline group, at day of 20, 24, 100 and 50μg OVA-challenged groups showed the bronchial hyperresponsiveness and the elevated numbers of inflammatory cells including eosinophils in BAL fluid, the alveolar and bronchial wall, as well as in bronchial lumen and blood vessels. Bronchial mucosal folds were increased, extended and thickened, with a large amount of mucous sputum plugs in the bronchial lumens and significant deposition of collagen fibers in the bronchial and blood vessels. Additionally, PAS staining showed increased mucus in bronchial lumen. Conclusion: With different doses of intranasal inhalation of OVA, we successfully established varying degrees of acute and sub-acute mouse models of asthma. Our studies provided the foundation for further research on the pathogenesis and drug screening of asthma using mouse models.