北京中医药大学学报
北京中醫藥大學學報
북경중의약대학학보
JOURNAL OF BEIJING UNIVERSITY OF TRADITIONAL CHINESE MEDICINE
2010年
1期
20-22,40
,共4页
丁建中%胡利群%张六通%王昌富%贺尚荣%王明明
丁建中%鬍利群%張六通%王昌富%賀尚榮%王明明
정건중%호리군%장륙통%왕창부%하상영%왕명명
外燥%纤毛-黏液毯%分泌型IgA%小鼠
外燥%纖毛-黏液毯%分泌型IgA%小鼠
외조%섬모-점액담%분비형IgA%소서
external dryness%cilium-mucous blanket%secretory IgA%mice
目的 动态观察外燥对小鼠气道局部御邪屏障的影响,研究外燥致病精细病理机制.方法 120只无特定病原体级(SPF)昆明种小鼠随机分为常温常湿组、常温燥组、温燥组、凉燥组,每组30只,分批置智能型人工气候箱、模拟外燥"温度-相对湿度-风"综合刺激进行造模.处理后第6、12、18天常规检测各组气管组织病理、气道液总蛋白(P)、气道液黏多糖(MS)和分泌型IgA(SIgA)含量.结果 常温燥组气道组织病变不明显;温燥组、凉燥组第6天至第18天气道上皮鳞状化生与纤毛缺损,20%~40%气管浆液腺上皮黏液腺化生,伴炎性细胞浸润,均以第12天为重.与燥相关3个组第12天至第18天P均减少,同期常温燥组MS呈升高趋势,温燥组MS与SIgA则持续下降(P<0.05),凉燥组第12天至第18天P持续下降(P<0.01),伴第12天MS减少(P<0.05).结论 温燥伤肺劫津,气不布津则气道组织失于濡润,伴SIgA持续减少进而加重病变,故减弱气道"纤毛-黏液毯"与局部免疫御邪屏障之功是外燥基本病机之一.第12天明显的气道病变将为研究外燥病机的"最佳观察期"提供依据.
目的 動態觀察外燥對小鼠氣道跼部禦邪屏障的影響,研究外燥緻病精細病理機製.方法 120隻無特定病原體級(SPF)昆明種小鼠隨機分為常溫常濕組、常溫燥組、溫燥組、涼燥組,每組30隻,分批置智能型人工氣候箱、模擬外燥"溫度-相對濕度-風"綜閤刺激進行造模.處理後第6、12、18天常規檢測各組氣管組織病理、氣道液總蛋白(P)、氣道液黏多糖(MS)和分泌型IgA(SIgA)含量.結果 常溫燥組氣道組織病變不明顯;溫燥組、涼燥組第6天至第18天氣道上皮鱗狀化生與纖毛缺損,20%~40%氣管漿液腺上皮黏液腺化生,伴炎性細胞浸潤,均以第12天為重.與燥相關3箇組第12天至第18天P均減少,同期常溫燥組MS呈升高趨勢,溫燥組MS與SIgA則持續下降(P<0.05),涼燥組第12天至第18天P持續下降(P<0.01),伴第12天MS減少(P<0.05).結論 溫燥傷肺劫津,氣不佈津則氣道組織失于濡潤,伴SIgA持續減少進而加重病變,故減弱氣道"纖毛-黏液毯"與跼部免疫禦邪屏障之功是外燥基本病機之一.第12天明顯的氣道病變將為研究外燥病機的"最佳觀察期"提供依據.
목적 동태관찰외조대소서기도국부어사병장적영향,연구외조치병정세병리궤제.방법 120지무특정병원체급(SPF)곤명충소서수궤분위상온상습조、상온조조、온조조、량조조,매조30지,분비치지능형인공기후상、모의외조"온도-상대습도-풍"종합자격진행조모.처리후제6、12、18천상규검측각조기관조직병리、기도액총단백(P)、기도액점다당(MS)화분비형IgA(SIgA)함량.결과 상온조조기도조직병변불명현;온조조、량조조제6천지제18천기도상피린상화생여섬모결손,20%~40%기관장액선상피점액선화생,반염성세포침윤,균이제12천위중.여조상관3개조제12천지제18천P균감소,동기상온조조MS정승고추세,온조조MS여SIgA칙지속하강(P<0.05),량조조제12천지제18천P지속하강(P<0.01),반제12천MS감소(P<0.05).결론 온조상폐겁진,기불포진칙기도조직실우유윤,반SIgA지속감소진이가중병변,고감약기도"섬모-점액담"여국부면역어사병장지공시외조기본병궤지일.제12천명현적기도병변장위연구외조병궤적"최가관찰기"제공의거.
Objective To observe dynamically the influence of external dryness on the local defend barrier in mouse airway, and study the pathogenic mechanism.Method Special pathogenic free (SPF) Kunming mice (n=120) were randomly divided into the normal-temperature and normal-dampness group (group A), normal-temperature and dryness group (group B), warm-dryness group (group C) and cool-dryness group (group D, each n=30). The mouse model was established by the synthetic stimulation of imitated external dryness of temperature-relevant humidity-wind in the intelligent artificial climate box. After 6, 12 and 18 days, the histopathological changes of respiratory tract, and the content of total protein(P), mucopolysaccharide (MS) and secretory IgA (SIgA) in the fluid of respiratory tract were detected respectively.Result The histopathological changes in airway was not obvious in group B. In group C and D there were squamous metaplasia of airway epithelium and cilium function defect, and epithelial mucous metaplasia of 20% to 40% trachea serous gland accompanied by the infiltration of inflammatory cells from the 6~(th) day to the 18~(th) day, which were the most serious on the 12~(th) day. The content of P decreased from the 12~(th) day to the 18~(th) day in group B, C and D, content of MS tended to increase in group B, and content of MS and SIgA decreased continuously in group C (P<0.05). The content of P decreased continuously in group D from the 12~(th) day to the 18~(th) day (P<0.05) and the content of MS decreased on the 12th day (P<0.05).Conclusion The result reconfirms TCM doctrine of warm-dryness inducing the impairment of lung, and the decrease of SIgA content aggravates the pathological changes. One of the basic pathogeneses of external dryness is related to the attenuation of cilium-mucous blanket and local defend barrier. The result also indicates that the obvious airway pathological changes on the 12~(th) day provides a base of the best observation phase for the research on the pathogenesis of external dryness.