中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2011年
2期
158-161
,共4页
郑美梅%江勇%温武金%王方剑%段成城%潘小华%董丽妍
鄭美梅%江勇%溫武金%王方劍%段成城%潘小華%董麗妍
정미매%강용%온무금%왕방검%단성성%반소화%동려연
叠氮红霉素/药理学%哮喘/药物疗法/代谢/病理生理学%气管/病理生理学/药物作用%转化生长因子β1/代谢
疊氮紅黴素/藥理學%哮喘/藥物療法/代謝/病理生理學%氣管/病理生理學/藥物作用%轉化生長因子β1/代謝
첩담홍매소/약이학%효천/약물요법/대사/병리생이학%기관/병리생이학/약물작용%전화생장인자β1/대사
Azithromycin/PD%Asthma/DT/ME/PP%Trachea/PP/DE%Transforming growth factor beta1/ME
目的 观察阿奇霉素对哮喘小鼠气道重构指标、转化生长因子-β1(transforming growth factor-β1,TGF-β1)表达的影响,探讨阿奇霉素对哮喘小鼠气道重构的影响.方法 30只雄性BALB/c小鼠随机分为正常对照组(A组)、哮喘模型组(B组)、阿奇霉素治疗组(C组),每组各10只,复制哮喘模型后收集支气管肺泡灌洗液(BALF),行白细胞(TOT),嗜酸性粒细胞(EOS)计数;医学图像分析软件观测支气管总管壁面积(Wat)、内壁面积(Wai)、平滑肌面积(Wam);SABC免疫组化法检测肺组织TGF-β1的表达.结果 B组BALF中嗜酸性粒细胞明显高于其他组(8.12±0.54 vs 0.70±0.40,8.12±0.54 vs 0.87±0.25,P<0.01);C组气道Wat、Wai、Wam均较B组减轻(10.15±0.95 vs 15.36±0.85,4.16±0.32 vs 10.64±1.03,3.77±0.15 vs 7.97±0.17,P<0.01),但较A组加重;B组TGF-β1(168.58±21.71 vs 130.47±18.22 vs 126.30±16.15)表达最强,C组减弱,A组微弱;TGF-β1的表达与EOS%(r=0.840,P<0.01)、Wat(r=0.735,P<0.01)、Wam(r=0.870,P<0.01)呈正相关.结论 阿奇霉素可抑制哮喘小鼠气道重构,可能是通过抑制TGF-β1的表达来实现的.
目的 觀察阿奇黴素對哮喘小鼠氣道重構指標、轉化生長因子-β1(transforming growth factor-β1,TGF-β1)錶達的影響,探討阿奇黴素對哮喘小鼠氣道重構的影響.方法 30隻雄性BALB/c小鼠隨機分為正常對照組(A組)、哮喘模型組(B組)、阿奇黴素治療組(C組),每組各10隻,複製哮喘模型後收集支氣管肺泡灌洗液(BALF),行白細胞(TOT),嗜痠性粒細胞(EOS)計數;醫學圖像分析軟件觀測支氣管總管壁麵積(Wat)、內壁麵積(Wai)、平滑肌麵積(Wam);SABC免疫組化法檢測肺組織TGF-β1的錶達.結果 B組BALF中嗜痠性粒細胞明顯高于其他組(8.12±0.54 vs 0.70±0.40,8.12±0.54 vs 0.87±0.25,P<0.01);C組氣道Wat、Wai、Wam均較B組減輕(10.15±0.95 vs 15.36±0.85,4.16±0.32 vs 10.64±1.03,3.77±0.15 vs 7.97±0.17,P<0.01),但較A組加重;B組TGF-β1(168.58±21.71 vs 130.47±18.22 vs 126.30±16.15)錶達最彊,C組減弱,A組微弱;TGF-β1的錶達與EOS%(r=0.840,P<0.01)、Wat(r=0.735,P<0.01)、Wam(r=0.870,P<0.01)呈正相關.結論 阿奇黴素可抑製哮喘小鼠氣道重構,可能是通過抑製TGF-β1的錶達來實現的.
목적 관찰아기매소대효천소서기도중구지표、전화생장인자-β1(transforming growth factor-β1,TGF-β1)표체적영향,탐토아기매소대효천소서기도중구적영향.방법 30지웅성BALB/c소서수궤분위정상대조조(A조)、효천모형조(B조)、아기매소치료조(C조),매조각10지,복제효천모형후수집지기관폐포관세액(BALF),행백세포(TOT),기산성립세포(EOS)계수;의학도상분석연건관측지기관총관벽면적(Wat)、내벽면적(Wai)、평활기면적(Wam);SABC면역조화법검측폐조직TGF-β1적표체.결과 B조BALF중기산성립세포명현고우기타조(8.12±0.54 vs 0.70±0.40,8.12±0.54 vs 0.87±0.25,P<0.01);C조기도Wat、Wai、Wam균교B조감경(10.15±0.95 vs 15.36±0.85,4.16±0.32 vs 10.64±1.03,3.77±0.15 vs 7.97±0.17,P<0.01),단교A조가중;B조TGF-β1(168.58±21.71 vs 130.47±18.22 vs 126.30±16.15)표체최강,C조감약,A조미약;TGF-β1적표체여EOS%(r=0.840,P<0.01)、Wat(r=0.735,P<0.01)、Wam(r=0.870,P<0.01)정정상관.결론 아기매소가억제효천소서기도중구,가능시통과억제TGF-β1적표체래실현적.
Objective To investigate the effects of azithromycin on airway remodeling and the expression of transforming growth factorβ1 (TGF-β1) in asthmatic mice.Methods BALB/c male mice were random divided into 3 groups:control group(A),asthma group (B),and azithromycin treated group (C),with 10 mice in each group.Bronchoalveolar lavage fluid was collected to count the number of white blood cells and eosinophilic granulocytes EOS.The morphological parameters of the bronchi were measured by computer image analysis and the pathologic changes of the bronchi and lung tissue were observed by HE staining.The expressions of TGF-β1 were detected by immunohistochemistry.Results The number of EOS in B group was significantly higher than that in control group(8.12 ±0.54 vs 0.70 ±0.40;8.12 ±0.54 vs 0.87 ±0.25,P <0.01).WAt and WAi and WAm in group C was significantly lower than that in group B (10.15 ±0.95 vs 15.36 ±0.85,4.16 ±0.32 vs 10.64 ± 1.03,3.77 ±0.15 vs 7.97 ±0.17,P <0.01)but higher than that in group A.The expression of TGF-β1 in group C was significantly lower than that in group B but higher than that in group A.TGF-β1 expression of lung tissue in C group was significantly correlated with EOS,(r =0.840,P <0.01) and WAt(r =0.735,P <0.01) and WAm (r =0.870,P <0.01).Conclusion Azithromycin inhibited airway remodeling in asthmatic mice,which might possibly be achieved through inhibiting the expression of TGF-β1.