中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
Chinese Journal of Pathophysiology
2015年
9期
1724-1728
,共5页
杜秀婷%罗良%谢宛君%肖志勋%卓桂锋%苏宁
杜秀婷%囉良%謝宛君%肖誌勛%卓桂鋒%囌寧
두수정%라량%사완군%초지훈%탁계봉%소저
慢性支气管炎%烟熏%二氧化硫%脂多糖
慢性支氣管炎%煙熏%二氧化硫%脂多糖
만성지기관염%연훈%이양화류%지다당
Chronic bronchitis%Smoking%Sulfur dioxide%Lipopolysaccharide
目的:结合慢性支气管炎的发病机制及致病因素,在以往单因素致病建模方法的基础上进行改良,探究一种较为准确、可靠、符合慢性支气管炎病理变化的模型。方法:慢支改良组(复合组)小鼠于实验第1、14天分别经气管和经鼻腔注入LPS,同时,于第2~30天(第14天除外)进行被动吸烟及SO2吸入;SO2组小鼠每天熏SO22 min;烟熏组小鼠每天吸烟4支/次,直至1包烟燃烧完毕,共约1 h;脂多糖组小鼠在造模第1天气管注入LPS,第14天、30天进行LPS滴鼻。各模型组均连续造模30 d。造模结束后通过对小鼠一般情况的观察、肺泡灌洗液结果分析以及支气管肺组织形态学观察等评价改良后的慢支模型。结果:造模后各模型组小鼠出现鼻部潮湿,咳嗽,体毛干枯无光泽,拱背蜷缩,少动,反应较为迟钝等症状,复合组的体质量增长最慢。从各组模型组病理切片可观察到细支气管壁周围有炎性细胞浸润,腔内炎性渗出明显,气道内分泌物增多等病变;与烟熏组、二氧化硫组比较,慢支改良组肺泡灌洗液白细胞总数显著增高( P<0.01);慢支改良组与其它3组比较肺组织炎症细胞浸润程度显著升高(P<0.01),且烟熏组与LPS组比较差异有统计学意义。结论:烟熏、二氧化硫、LPS均可导致小鼠慢支疾病的发生,而从支气管及肺组织病理学、肺泡灌洗液细胞学以及慢支的发病学等方面分析,复合因素造模更为符合慢支模型的构建。
目的:結閤慢性支氣管炎的髮病機製及緻病因素,在以往單因素緻病建模方法的基礎上進行改良,探究一種較為準確、可靠、符閤慢性支氣管炎病理變化的模型。方法:慢支改良組(複閤組)小鼠于實驗第1、14天分彆經氣管和經鼻腔註入LPS,同時,于第2~30天(第14天除外)進行被動吸煙及SO2吸入;SO2組小鼠每天熏SO22 min;煙熏組小鼠每天吸煙4支/次,直至1包煙燃燒完畢,共約1 h;脂多糖組小鼠在造模第1天氣管註入LPS,第14天、30天進行LPS滴鼻。各模型組均連續造模30 d。造模結束後通過對小鼠一般情況的觀察、肺泡灌洗液結果分析以及支氣管肺組織形態學觀察等評價改良後的慢支模型。結果:造模後各模型組小鼠齣現鼻部潮濕,咳嗽,體毛榦枯無光澤,拱揹踡縮,少動,反應較為遲鈍等癥狀,複閤組的體質量增長最慢。從各組模型組病理切片可觀察到細支氣管壁週圍有炎性細胞浸潤,腔內炎性滲齣明顯,氣道內分泌物增多等病變;與煙熏組、二氧化硫組比較,慢支改良組肺泡灌洗液白細胞總數顯著增高( P<0.01);慢支改良組與其它3組比較肺組織炎癥細胞浸潤程度顯著升高(P<0.01),且煙熏組與LPS組比較差異有統計學意義。結論:煙熏、二氧化硫、LPS均可導緻小鼠慢支疾病的髮生,而從支氣管及肺組織病理學、肺泡灌洗液細胞學以及慢支的髮病學等方麵分析,複閤因素造模更為符閤慢支模型的構建。
목적:결합만성지기관염적발병궤제급치병인소,재이왕단인소치병건모방법적기출상진행개량,탐구일충교위준학、가고、부합만성지기관염병리변화적모형。방법:만지개량조(복합조)소서우실험제1、14천분별경기관화경비강주입LPS,동시,우제2~30천(제14천제외)진행피동흡연급SO2흡입;SO2조소서매천훈SO22 min;연훈조소서매천흡연4지/차,직지1포연연소완필,공약1 h;지다당조소서재조모제1천기관주입LPS,제14천、30천진행LPS적비。각모형조균련속조모30 d。조모결속후통과대소서일반정황적관찰、폐포관세액결과분석이급지기관폐조직형태학관찰등평개개량후적만지모형。결과:조모후각모형조소서출현비부조습,해수,체모간고무광택,공배권축,소동,반응교위지둔등증상,복합조적체질량증장최만。종각조모형조병리절편가관찰도세지기관벽주위유염성세포침윤,강내염성삼출명현,기도내분비물증다등병변;여연훈조、이양화류조비교,만지개량조폐포관세액백세포총수현저증고( P<0.01);만지개량조여기타3조비교폐조직염증세포침윤정도현저승고(P<0.01),차연훈조여LPS조비교차이유통계학의의。결론:연훈、이양화류、LPS균가도치소서만지질병적발생,이종지기관급폐조직병이학、폐포관세액세포학이급만지적발병학등방면분석,복합인소조모경위부합만지모형적구건。
AIM:To explore a more accurate and reliable pathological model of the chronic bronchitis , which has improved from the former single-factor modeling method of the disease .METHODS:The mice in complex group were treated with lipopolysaccharide ( LPS) by tracheal injection on the 1st day and nasal drops on the 14th day, and from the 2nd day to 30th day, the animals were given passive smoking and sulfur dioxide ( SO2 ) inhalation ( except on the 14th day).The mice in SO2 group were exposed to SO2 2 min per day, while in smoking group, the mice were exposed to smoke for about 1 h per day (4 cigarettes each time until one pack of cigarettes were burning up ).In LPS group, the mice had tracheal injection of LPS on the 1st day and nasal drops of LPS on the 14th day and 30th day.Every modeling process las-ted for 30 days.After modeling, the improvement of chronic bronchitis model was evaluated by testing the general condi-tions of the mice , analyzing leukocyte count in bronchoalveolar lavage fluid ( BALF ) , and observing the morphological changes of the bronchial and lung tissues .RESULTS:After modeling, the mice in every model group experienced symp-toms including wet nose, cough, dry and lusterless hair, arched back and curled-up body, showing inactive, and slow down in response .The mice in complex group gained the lowest weight compared to other groups .From each model group , the inflammatory cells infiltrated evidently around the bronchial walls , especially in the bronchial cavity , and the mucilage secretion in the airway increased .The total number of leukocytes in BALF increased significantly in complex group .The in-flammatory cell count in the lung tissue indicated that the mice in complex group had significantly higher levels of inflamma -tory cell infiltration.Besides, the comparison between smoke group and LPS group was statistically significant .CONCLU-SION:Smoking, SO2 inhalation and LPS injection induce bronchial lung disease in mice , and the complex chronic bron-chitis mouse model is a better model with the pathological changes of bronchus , lung tissue and BALF , and pathogenesis of chronic bronchitis .