中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2010年
5期
325-328
,共4页
张大勇%黄中新%蒋立娣%楼雪芳%姚雪燕
張大勇%黃中新%蔣立娣%樓雪芳%姚雪燕
장대용%황중신%장립제%루설방%요설연
正己烷%肺损伤%Clara细胞分泌蛋白%溶菌酶
正己烷%肺損傷%Clara細胞分泌蛋白%溶菌酶
정기완%폐손상%Clara세포분비단백%용균매
n-hexane%Lung injury%Clara cell secretory protein%Muramidase
目的 观察正己烷慢性吸入致昆明种小鼠肺损伤中Clara细胞分泌蛋白(clara cell secretory protein,CCSP)的表达情况,探讨Clara细胞在正己烷慢性吸入致肺损伤中的作用.方法 24只昆明种小鼠随机分为4组(正常对照组及染毒4周、8周、12周组),初始正已烷染毒浓度为17.6g/m3,每天8 h,每周染毒6 d.染毒结束后即刻处死,气相色谱-质谱联用仪测全血中正己烷浓度.对肺组织进行HE染色,观察光学显微镜下肺组织形态学变化,免疫组织化学法观察细支气管内CCSP阳性反应的Clara细胞比例及肺组织内溶菌酶阳性反应的巨噬细胞数量变化.结果 各染毒组小鼠血中正己烷平均浓度均明显高于对照组,差异均有统计学意义(P＜0.01).各染毒组小鼠肺脏出现进行性的间质性炎症反应.染毒4周、8周和12周组Clara细胞在终末性细支气管和呼吸性细支气管上皮细胞中比例分别为(73.33±4.21)%、(60.98±4.94)%、(34.04±2.33)%和(75.44±7.91)%、(58.54±4.86)%、(33.35±2.67)%,较对照组[(80.26±6.43)%和(81.74±7.75)%]明显下降,差异均有统计学意义(P＜0.05或P＜0.01),各染毒组肺组织内巨噬细胞数量分别为(21.39±7.41)、(28.54±10.73)、(48.97±19.55)个/视野,较对照组[(7.84±3.12)个/视野]明显增多,且随染毒时间延长,巨噬细胞数量呈增加的趋势,差异均有统计学意义(P＜0.05或P＜0.01).结论 慢性吸入正已烷可致昆明种小鼠细支气管上皮内Clara细胞持续受损,进而引起肺脏慢性炎症.
目的 觀察正己烷慢性吸入緻昆明種小鼠肺損傷中Clara細胞分泌蛋白(clara cell secretory protein,CCSP)的錶達情況,探討Clara細胞在正己烷慢性吸入緻肺損傷中的作用.方法 24隻昆明種小鼠隨機分為4組(正常對照組及染毒4週、8週、12週組),初始正已烷染毒濃度為17.6g/m3,每天8 h,每週染毒6 d.染毒結束後即刻處死,氣相色譜-質譜聯用儀測全血中正己烷濃度.對肺組織進行HE染色,觀察光學顯微鏡下肺組織形態學變化,免疫組織化學法觀察細支氣管內CCSP暘性反應的Clara細胞比例及肺組織內溶菌酶暘性反應的巨噬細胞數量變化.結果 各染毒組小鼠血中正己烷平均濃度均明顯高于對照組,差異均有統計學意義(P＜0.01).各染毒組小鼠肺髒齣現進行性的間質性炎癥反應.染毒4週、8週和12週組Clara細胞在終末性細支氣管和呼吸性細支氣管上皮細胞中比例分彆為(73.33±4.21)%、(60.98±4.94)%、(34.04±2.33)%和(75.44±7.91)%、(58.54±4.86)%、(33.35±2.67)%,較對照組[(80.26±6.43)%和(81.74±7.75)%]明顯下降,差異均有統計學意義(P＜0.05或P＜0.01),各染毒組肺組織內巨噬細胞數量分彆為(21.39±7.41)、(28.54±10.73)、(48.97±19.55)箇/視野,較對照組[(7.84±3.12)箇/視野]明顯增多,且隨染毒時間延長,巨噬細胞數量呈增加的趨勢,差異均有統計學意義(P＜0.05或P＜0.01).結論 慢性吸入正已烷可緻昆明種小鼠細支氣管上皮內Clara細胞持續受損,進而引起肺髒慢性炎癥.
목적 관찰정기완만성흡입치곤명충소서폐손상중Clara세포분비단백(clara cell secretory protein,CCSP)적표체정황,탐토Clara세포재정기완만성흡입치폐손상중적작용.방법 24지곤명충소서수궤분위4조(정상대조조급염독4주、8주、12주조),초시정이완염독농도위17.6g/m3,매천8 h,매주염독6 d.염독결속후즉각처사,기상색보-질보련용의측전혈중정기완농도.대폐조직진행HE염색,관찰광학현미경하폐조직형태학변화,면역조직화학법관찰세지기관내CCSP양성반응적Clara세포비례급폐조직내용균매양성반응적거서세포수량변화.결과 각염독조소서혈중정기완평균농도균명현고우대조조,차이균유통계학의의(P＜0.01).각염독조소서폐장출현진행성적간질성염증반응.염독4주、8주화12주조Clara세포재종말성세지기관화호흡성세지기관상피세포중비례분별위(73.33±4.21)%、(60.98±4.94)%、(34.04±2.33)%화(75.44±7.91)%、(58.54±4.86)%、(33.35±2.67)%,교대조조[(80.26±6.43)%화(81.74±7.75)%]명현하강,차이균유통계학의의(P＜0.05혹P＜0.01),각염독조폐조직내거서세포수량분별위(21.39±7.41)、(28.54±10.73)、(48.97±19.55)개/시야,교대조조[(7.84±3.12)개/시야]명현증다,차수염독시간연장,거서세포수량정증가적추세,차이균유통계학의의(P＜0.05혹P＜0.01).결론 만성흡입정이완가치곤명충소서세지기관상피내Clara세포지속수손,진이인기폐장만성염증.
Objective To observe the expression of Clara cell secretory protein (CCSP) in the Kunming mouse model of n-hexane long-term inhalation, and to discuss the functions of Clara cell in injury lung induced by n-hexane. Methods 24 healthy mice were randomly divided into 4 groups: one control group and three nhexane groups (4 w, 8 w and 12 w), 6 each group. Primary concentration of n-hexane was 17.6 g/m3,8 hours per day, 6 d per week. After inhalation, n-hexane concentration of blood from celiac artery was detected. The lungs were embedded with paraffin and HE staining in the routine. The ratio of Clara cells with CCSP reaction in bronchiole and the number of macrophage cells with lysozyme reaction were determined by immuno-histochemistry.Results In the poisoning groups, the average n-hexane concentration of blood was significantly higher than that of the control group (P＜0.01). There were apparent pathologic damages in lungs of the poisoning mice. In poisoning 4 w,8 w and 12 w groups,the ratio of Clara cells was significantly decreased [(73.33±4.21)%,(60.98±4.94)%,(34.04±2.33)%in terminal bronchiole,and(75.44±7.91)%,(58.54±4.86)%,(33.35±2.67)%in respiratory bronchiolel as compared with the control mice[(80.26±6.43)%and(81.74±7.75)%,P＜0.05 or P＜0.011,meanwhile the numbers of macrophage cells were gradually increased[(21.39±7.41),(28.54±10.73),(48.97±19.55)per microscopic field at 200×]in poisoning mice than those in control mice[(7.84±3.12)per microscopie field at 200×,P＜0.05 or P＜0.01].Conclusion In injury lungs after n-hexane inhalation,Clara cells are the target cells of n-hexane toxicity effect.Clara cells play an extensive protective role in lung inflammation.
