实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
22期
3548-3551
,共4页
孙天寿%易桂生%郑红%刘凯静
孫天壽%易桂生%鄭紅%劉凱靜
손천수%역계생%정홍%류개정
哮喘%慢性应激%疏肝理肺%TGF-β1%Smad3
哮喘%慢性應激%疏肝理肺%TGF-β1%Smad3
효천%만성응격%소간리폐%TGF-β1%Smad3
Asthma%Chronicstress condition%Shugan Lifei%TGF-β1%Smad3
目的:探讨疏肝理肺方对慢性应激条件下哮喘大鼠肺组织TGF-β1和Smad3表达的影响。方法:将40只SD雄性大鼠随机分为正常对照组、应激哮喘组、地塞米松组、疏肝理肺组。采用卵蛋白(OVA)致敏激发哮喘,同时加慢性不可预见性温和应激法(CUMS)复制慢性应激条件下哮喘大鼠模型,第15天开始,治疗组每天以地塞米松及疏肝理肺方灌胃。 HE染色作肺组织病理学观察,免疫组化及逆转录-聚合酶链反应(RT-PCR)法测定肺组织TGF-β1及Smad3的表达水平。结果:应激哮喘组大鼠支气管壁面积和气道平滑肌面积较正常对照组增厚;与其相比,地塞米松组及疏肝理肺组明显降低。与正常对照组相比,应激哮喘组大鼠肺组织 TGF-β1及 Smad3的蛋白和 mRNA 表达均明显升高(P <0.05);地塞米松及疏肝理肺组TGF-β1及Smad3的蛋白和mRNA表达较应激哮喘组显著降低(P<0.05)。结论:疏肝理肺法具有改善慢性应激条件下哮喘大鼠模型气道重塑的作用,此作用可能通过减少TGF-β1及Smad3的表达而实现。
目的:探討疏肝理肺方對慢性應激條件下哮喘大鼠肺組織TGF-β1和Smad3錶達的影響。方法:將40隻SD雄性大鼠隨機分為正常對照組、應激哮喘組、地塞米鬆組、疏肝理肺組。採用卵蛋白(OVA)緻敏激髮哮喘,同時加慢性不可預見性溫和應激法(CUMS)複製慢性應激條件下哮喘大鼠模型,第15天開始,治療組每天以地塞米鬆及疏肝理肺方灌胃。 HE染色作肺組織病理學觀察,免疫組化及逆轉錄-聚閤酶鏈反應(RT-PCR)法測定肺組織TGF-β1及Smad3的錶達水平。結果:應激哮喘組大鼠支氣管壁麵積和氣道平滑肌麵積較正常對照組增厚;與其相比,地塞米鬆組及疏肝理肺組明顯降低。與正常對照組相比,應激哮喘組大鼠肺組織 TGF-β1及 Smad3的蛋白和 mRNA 錶達均明顯升高(P <0.05);地塞米鬆及疏肝理肺組TGF-β1及Smad3的蛋白和mRNA錶達較應激哮喘組顯著降低(P<0.05)。結論:疏肝理肺法具有改善慢性應激條件下哮喘大鼠模型氣道重塑的作用,此作用可能通過減少TGF-β1及Smad3的錶達而實現。
목적:탐토소간리폐방대만성응격조건하효천대서폐조직TGF-β1화Smad3표체적영향。방법:장40지SD웅성대서수궤분위정상대조조、응격효천조、지새미송조、소간리폐조。채용란단백(OVA)치민격발효천,동시가만성불가예견성온화응격법(CUMS)복제만성응격조건하효천대서모형,제15천개시,치료조매천이지새미송급소간리폐방관위。 HE염색작폐조직병이학관찰,면역조화급역전록-취합매련반응(RT-PCR)법측정폐조직TGF-β1급Smad3적표체수평。결과:응격효천조대서지기관벽면적화기도평활기면적교정상대조조증후;여기상비,지새미송조급소간리폐조명현강저。여정상대조조상비,응격효천조대서폐조직 TGF-β1급 Smad3적단백화 mRNA 표체균명현승고(P <0.05);지새미송급소간리폐조TGF-β1급Smad3적단백화mRNA표체교응격효천조현저강저(P<0.05)。결론:소간리폐법구유개선만성응격조건하효천대서모형기도중소적작용,차작용가능통과감소TGF-β1급Smad3적표체이실현。
Objective To explore the effect of Shugan Lifei prescription on expression of Transforming Growth Factor-beta1(TGF-β1) and Smad3 in asthma rats under chronic stress condition. Method The 40 SD rats were randomly divided into four groups:control group, model group, dexamethasone group and Shugan Lifei group. Asthma model was established by inhaling atomized ovalbumin (OVA) passively and experiencing chronic unpredictable mild stress (CUMS). From the 15th day of modeling, the treatment groups were intervened with dexamethasone drugs and Shugan Lifei prescription. Lung pathomorphology was observed via HE staining. The expressions of TGF-β1 and Smad3 in lung tissue were measured by immunohistochemical and RT-PCR. Results Compared with control group, the wall area and the smooth muscle area in the model group significantly increased. While compared with asthmatic model group,the wall area and the smooth muscle area in the dexamethasone group and Shugan Lifei group were significantly lower. Immunohistochemistry and RT-PCR showed that in comparison with control group , the expression of TGF-β1/Smad3 protein and mRNA in lung tissues in the model group significantly increased(P<0.05), while the TGF-β1/Smad3 protein and mRNA in lung tissues in the dexamethasone group and Shugan Lifei group were detected to be significantly lower than model group (P<0.05). Conclusion Shugan Lifei method could improve airway remodeling in asthma rats under chronic stress condition , and this result is possibly achieved by reducing TGF-β1 and Smad3 expression levels.