中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2011年
8期
826-829
,共4页
董雪松%刘盛业%刘伟%刘淑英%刘志
董雪鬆%劉盛業%劉偉%劉淑英%劉誌
동설송%류성업%류위%류숙영%류지
百草枯%中毒%肺间质纤维化%转化生长因子-β1%巨噬细胞%图像分析
百草枯%中毒%肺間質纖維化%轉化生長因子-β1%巨噬細胞%圖像分析
백초고%중독%폐간질섬유화%전화생장인자-β1%거서세포%도상분석
Paraquat%Intoxication%Pulmonary fibrosis%Transforming growth factor-β1%Macrophages%Image analysis
目的 用免疫组织化学的方法观察百草枯(PQ)致肺间质纤维化过程中转化生长因子-β1(TGF-β1)的表达。方法 58只雄性C57BL/6J小鼠随机(随机数字法)分组。实验组48只,通过腹腔注射PQ(10 mg/kg)建立小鼠肺间质纤维化模型;对照组10只,腹腔注射等量生理盐水。实验组染毒后2,5,7,14 d和对照组7d时小鼠分别被处死,留取肺组织标本。标本进一步进行HE染色和TGF-β1的免疫组化研究,并进行TGF-β1的积分光密度(iOD)分析,两组间的数据比较采用成组t检验。结果 PQ致肺纤维化过程中,巨噬细胞中TGF-β1表达显著增加。随着纤维化进程的进展,TGF-β1染色阳性主要见于浸润的巨噬细胞和中性粒细胞的胞浆中。染毒后14 d,除了巨噬细胞外,TGF-β1染色阳性也见于成纤维细胞灶中的成纤维细胞和肌成纤维细胞。与对照组相比,实验组各时间点TGF-β1的积分光密度在纤维化开始后明显增加(P<0.01)并呈上升趋势。结论 在PQ致肺间质纤维化过程中,TGF-β1的表达显著增加并对肺纤维化的发生发展具有重要的作用。
目的 用免疫組織化學的方法觀察百草枯(PQ)緻肺間質纖維化過程中轉化生長因子-β1(TGF-β1)的錶達。方法 58隻雄性C57BL/6J小鼠隨機(隨機數字法)分組。實驗組48隻,通過腹腔註射PQ(10 mg/kg)建立小鼠肺間質纖維化模型;對照組10隻,腹腔註射等量生理鹽水。實驗組染毒後2,5,7,14 d和對照組7d時小鼠分彆被處死,留取肺組織標本。標本進一步進行HE染色和TGF-β1的免疫組化研究,併進行TGF-β1的積分光密度(iOD)分析,兩組間的數據比較採用成組t檢驗。結果 PQ緻肺纖維化過程中,巨噬細胞中TGF-β1錶達顯著增加。隨著纖維化進程的進展,TGF-β1染色暘性主要見于浸潤的巨噬細胞和中性粒細胞的胞漿中。染毒後14 d,除瞭巨噬細胞外,TGF-β1染色暘性也見于成纖維細胞竈中的成纖維細胞和肌成纖維細胞。與對照組相比,實驗組各時間點TGF-β1的積分光密度在纖維化開始後明顯增加(P<0.01)併呈上升趨勢。結論 在PQ緻肺間質纖維化過程中,TGF-β1的錶達顯著增加併對肺纖維化的髮生髮展具有重要的作用。
목적 용면역조직화학적방법관찰백초고(PQ)치폐간질섬유화과정중전화생장인자-β1(TGF-β1)적표체。방법 58지웅성C57BL/6J소서수궤(수궤수자법)분조。실험조48지,통과복강주사PQ(10 mg/kg)건립소서폐간질섬유화모형;대조조10지,복강주사등량생리염수。실험조염독후2,5,7,14 d화대조조7d시소서분별피처사,류취폐조직표본。표본진일보진행HE염색화TGF-β1적면역조화연구,병진행TGF-β1적적분광밀도(iOD)분석,량조간적수거비교채용성조t검험。결과 PQ치폐섬유화과정중,거서세포중TGF-β1표체현저증가。수착섬유화진정적진전,TGF-β1염색양성주요견우침윤적거서세포화중성립세포적포장중。염독후14 d,제료거서세포외,TGF-β1염색양성야견우성섬유세포조중적성섬유세포화기성섬유세포。여대조조상비,실험조각시간점TGF-β1적적분광밀도재섬유화개시후명현증가(P<0.01)병정상승추세。결론 재PQ치폐간질섬유화과정중,TGF-β1적표체현저증가병대폐섬유화적발생발전구유중요적작용。
Objective To study the changes of transforming growth factor-β1 (TGF-β1) in pulmonary fibrosis induced by paraquat (PQ) with immunohistochemistry method. Methods A total of 58 C57BL/6J male mice were randomly (random number) divided into the experimental group and control group. Pulmonary fibrosis was induced by intra-peritoneal injection of PQ in dose of 10 mg/kg into the mice of experimental group (n = 48), while physiological saline was used instead in mice of control group (n = 10). The mice of experimental group were sacrificed 2, 5, 7 and 14 days after PQ poisoning and the mice of control group were sacrificed on the 7th day after saline administration. Lungs of mice were taken and histological changes in lungs were evaluated by haematoxylin-eosin stain, and TGF-β1 was determined with immunohistochemistry method. The integrated optical density (iOD) value of TGF-β1 was measured and analyzed. Results The TGF-β1 was markedly increased in macrophages during the genesis of pulmonary fibrosis induced by PQ. As the course of fibrosis progressed, the positive staining of TGF-B1 was mainly seen in macrophages and neutrophil's cytoplasm. On the 14th day after PQ poisoning, TGF-β1-positive cells were also detected in the fibroblast and myo-fibroblast inside the fibroblastic foci. Compared with the control group, the iOD value of TGF-β1 increased in experimental group (P < 0. 01 ) and it gradually upgraded during the course of fibrosis. Conclusions The TGF-β1 significantly increased during the course of pulmonary fibrosis induced by PQ and played an important role in the pathogenesis of the disease.