风湿病与关节炎
風濕病與關節炎
풍습병여관절염
Rheumatism and Arthritis
2014年
6期
19-22,38
,共5页
伍婷%楚海燕%史颖%刘庆梅%郭刚%王久存
伍婷%楚海燕%史穎%劉慶梅%郭剛%王久存
오정%초해연%사영%류경매%곽강%왕구존
肺纤维化%参麦开肺散%胶原%细胞外基质%纤维化基因%小鼠
肺纖維化%參麥開肺散%膠原%細胞外基質%纖維化基因%小鼠
폐섬유화%삼맥개폐산%효원%세포외기질%섬유화기인%소서
pulmonary ifbrosis%Shenmai Kaifei Powder%collagen%extracellular matrix%ifbrosis gene%mice
目的：利用博莱霉素诱导的肺纤维化小鼠模型研究参麦开肺散对胶原生成的影响。方法：将6～8周龄C57BL/6小鼠单次气管灌注浓度为2.5 mg·kg-1的博莱霉素，建立肺纤维化模型；24只小鼠随机平均分为预防组和治疗组，两组分别包括对照组、模型组和药物组。从小鼠肺组织病理切片、肺组织胶原含量、胶原基因表达量、细胞外基质基因表达量等4个方面研究参麦开肺散在缓解肺纤维化过程中对胶原生成的影响。结果：无论是预防组还是治疗组，对照组中小鼠肺组织均无明显病理变化，模型组小鼠肺泡结构破坏，炎症细胞浸润，并有大量以胶原为主的细胞外基质沉积，表现出了严重的纤维化病变。经过药物治疗，小鼠肺泡结构接近正常，且细胞外基质沉积现象明显缓解；实时定量PCR结果显示，模型组小鼠肺组织中胶原基因Col1a1、Col1a2、Col3a1表达量显著升高，喂食药物后，胶原基因表达量大幅度下调。此外，模型组中细胞外基质基因如Ctgf、Fn1、Sparc、Tgf-β1的表达量相对于对照组均有所升高，而喂食药物之后其表达量均有所下调。结论：参麦开肺散通过降低相关纤维化基因如Ctgf、Fn1、Sparc、Tgf-β1的表达而有效减少胶原的生成，缓解纤维化进程。
目的：利用博萊黴素誘導的肺纖維化小鼠模型研究參麥開肺散對膠原生成的影響。方法：將6～8週齡C57BL/6小鼠單次氣管灌註濃度為2.5 mg·kg-1的博萊黴素，建立肺纖維化模型；24隻小鼠隨機平均分為預防組和治療組，兩組分彆包括對照組、模型組和藥物組。從小鼠肺組織病理切片、肺組織膠原含量、膠原基因錶達量、細胞外基質基因錶達量等4箇方麵研究參麥開肺散在緩解肺纖維化過程中對膠原生成的影響。結果：無論是預防組還是治療組，對照組中小鼠肺組織均無明顯病理變化，模型組小鼠肺泡結構破壞，炎癥細胞浸潤，併有大量以膠原為主的細胞外基質沉積，錶現齣瞭嚴重的纖維化病變。經過藥物治療，小鼠肺泡結構接近正常，且細胞外基質沉積現象明顯緩解；實時定量PCR結果顯示，模型組小鼠肺組織中膠原基因Col1a1、Col1a2、Col3a1錶達量顯著升高，餵食藥物後，膠原基因錶達量大幅度下調。此外，模型組中細胞外基質基因如Ctgf、Fn1、Sparc、Tgf-β1的錶達量相對于對照組均有所升高，而餵食藥物之後其錶達量均有所下調。結論：參麥開肺散通過降低相關纖維化基因如Ctgf、Fn1、Sparc、Tgf-β1的錶達而有效減少膠原的生成，緩解纖維化進程。
목적：이용박래매소유도적폐섬유화소서모형연구삼맥개폐산대효원생성적영향。방법：장6～8주령C57BL/6소서단차기관관주농도위2.5 mg·kg-1적박래매소，건립폐섬유화모형；24지소서수궤평균분위예방조화치료조，량조분별포괄대조조、모형조화약물조。종소서폐조직병리절편、폐조직효원함량、효원기인표체량、세포외기질기인표체량등4개방면연구삼맥개폐산재완해폐섬유화과정중대효원생성적영향。결과：무론시예방조환시치료조，대조조중소서폐조직균무명현병리변화，모형조소서폐포결구파배，염증세포침윤，병유대량이효원위주적세포외기질침적，표현출료엄중적섬유화병변。경과약물치료，소서폐포결구접근정상，차세포외기질침적현상명현완해；실시정량PCR결과현시，모형조소서폐조직중효원기인Col1a1、Col1a2、Col3a1표체량현저승고，위식약물후，효원기인표체량대폭도하조。차외，모형조중세포외기질기인여Ctgf、Fn1、Sparc、Tgf-β1적표체량상대우대조조균유소승고，이위식약물지후기표체량균유소하조。결론：삼맥개폐산통과강저상관섬유화기인여Ctgf、Fn1、Sparc、Tgf-β1적표체이유효감소효원적생성，완해섬유화진정。
[ABSTRACT]Objective:To study the effects of Shenmai Kaifei Powder on collagenation in bleomycin-induced mice models with pulmonary ifbrosis.Methods:6~8-week-old C57BL/6 mice were given intratracheal instillation of bleomycin with the concentration of 2.5 mg·kg-1 to induce models with pulmonary ifbrosis;24 mice were randomly divided into the prevention group and the treatment group,respectively including the control group,the model group and the drug group.Studied the effects of Shenmai Kaifei Powder on collagenation in relieving pulmonary fibrosis from 4 aspects:pathological section of the mouse lung tissue,collagen content of the lung tissue,collagen gene expression and extracellular matrix gene expression.Results:No matter in the the prevention group or the treatment group,the lung tissue of the control group showed no signiifcant pathological changes,while in the model group,there were damage of alveolar structure,inflammatory cell infiltration and a large amount of extracellular matrix deposition composed mainly of collagen,showing a severe fibrosis.After treatment,the mouse alveolar structure recovered to normal and extracellular matrix deposition was alleviated;the results of real-time quantitative PCR showed a signiifcant increase of Col1a1,Col1a2 and Col3a1 expressions in the lung tissue of the model group.After feeding drugs,collagen gene expression significantly decreased.In addition,the expressions of extracellular matrix genes such as Ctgf,Fn1,Sparc and Tgf- β1in the model group increased compared with those of the control group,while the expressions reduced after giving drugs. Conclusion:Shenmai Kaifei Powder can effectively reduce the formation of collagen by reducing the expressions of related ifbrosis genes such as Ctgf,Fn1,Sparc and Tgf-β1,slowing the process of ifbrosis.
