临床儿科杂志
臨床兒科雜誌
림상인과잡지
2013年
11期
1070-1073
,共4页
肺动脉高压%野百合碱%全反式维甲酸%α-平滑肌肌动蛋白
肺動脈高壓%野百閤堿%全反式維甲痠%α-平滑肌肌動蛋白
폐동맥고압%야백합감%전반식유갑산%α-평활기기동단백
pulmonary arterial hypertension%monocrotaline%all-trans retinoic acid%α-smooth muscle actin
目的：通过全反式维甲酸（ATRA）在肺动脉高压大鼠中对α-平滑肌肌动蛋白（α-SMA）表达的影响，探讨ATRA治疗肺动脉高压可能机制。方法将30只雄性SD大鼠，随机分为对照组、模型组、干预组，每组10只。模型组和干预组大鼠腹腔一次性注射野百合碱，60 mg/kg，制作肺动脉高压模型；干预组于制模当天起，每天一次给予ATRA灌胃，30 mg/(kg·d)，连续28 d。第28天检测各组大鼠肺动脉平均压、右心室肥厚指数（RVHI），测定肺小动脉管壁厚度占动脉外径的百分比（WT%）及管壁面积占血管总面积的百分比（WA%）。实时荧光定量PCR和Western blot检测α-SMA mRNA及蛋白在肺组织中的表达。结果模型组大鼠的肺动脉平均压、RVHI和WT%、WA%均显著高于干预组和对照组，干预组亦均高于对照组，差异有统计学意义（P均<0.01）。模型组大鼠肺组织中α-SMA mRNA和蛋白表达水平显著高于对照组和干预组，差异有统计学意义（P<0.01），而干预组与对照组的差异无统计学意义（P>0.05）。结论 ATRA可抑制野百合碱诱导的大鼠肺动脉高压模型中肺组织α-SMA mRNA和蛋白的表达，对肺动脉高压可能有治疗作用。
目的：通過全反式維甲痠（ATRA）在肺動脈高壓大鼠中對α-平滑肌肌動蛋白（α-SMA）錶達的影響，探討ATRA治療肺動脈高壓可能機製。方法將30隻雄性SD大鼠，隨機分為對照組、模型組、榦預組，每組10隻。模型組和榦預組大鼠腹腔一次性註射野百閤堿，60 mg/kg，製作肺動脈高壓模型；榦預組于製模噹天起，每天一次給予ATRA灌胃，30 mg/(kg·d)，連續28 d。第28天檢測各組大鼠肺動脈平均壓、右心室肥厚指數（RVHI），測定肺小動脈管壁厚度佔動脈外徑的百分比（WT%）及管壁麵積佔血管總麵積的百分比（WA%）。實時熒光定量PCR和Western blot檢測α-SMA mRNA及蛋白在肺組織中的錶達。結果模型組大鼠的肺動脈平均壓、RVHI和WT%、WA%均顯著高于榦預組和對照組，榦預組亦均高于對照組，差異有統計學意義（P均<0.01）。模型組大鼠肺組織中α-SMA mRNA和蛋白錶達水平顯著高于對照組和榦預組，差異有統計學意義（P<0.01），而榦預組與對照組的差異無統計學意義（P>0.05）。結論 ATRA可抑製野百閤堿誘導的大鼠肺動脈高壓模型中肺組織α-SMA mRNA和蛋白的錶達，對肺動脈高壓可能有治療作用。
목적：통과전반식유갑산（ATRA）재폐동맥고압대서중대α-평활기기동단백（α-SMA）표체적영향，탐토ATRA치료폐동맥고압가능궤제。방법장30지웅성SD대서，수궤분위대조조、모형조、간예조，매조10지。모형조화간예조대서복강일차성주사야백합감，60 mg/kg，제작폐동맥고압모형；간예조우제모당천기，매천일차급여ATRA관위，30 mg/(kg·d)，련속28 d。제28천검측각조대서폐동맥평균압、우심실비후지수（RVHI），측정폐소동맥관벽후도점동맥외경적백분비（WT%）급관벽면적점혈관총면적적백분비（WA%）。실시형광정량PCR화Western blot검측α-SMA mRNA급단백재폐조직중적표체。결과모형조대서적폐동맥평균압、RVHI화WT%、WA%균현저고우간예조화대조조，간예조역균고우대조조，차이유통계학의의（P균<0.01）。모형조대서폐조직중α-SMA mRNA화단백표체수평현저고우대조조화간예조，차이유통계학의의（P<0.01），이간예조여대조조적차이무통계학의의（P>0.05）。결론 ATRA가억제야백합감유도적대서폐동맥고압모형중폐조직α-SMA mRNA화단백적표체，대폐동맥고압가능유치료작용。
Objectives To explore the possible mechanism of all-trans-retinoic acid (ATRA) therapy for pulmonary ar-terial hypertension by observing the effect of ATRA on the expression ofα-smooth muscle actin (α-SMA) in monocrotaline (MCT)-induced rats with pulmonary hypertension. Methods Thirty SD rats were randomly divided into control group, MCT-induced pulmonary hypertension group (model group) and ATRA treatment group (therapeutic group). MCT (60mg/kg) was injected to the rats in the model group and the therapeutic group to induce pulmonary arterial hypertension. And at the same day ATRA [30mg/(kg?d)] was given to rats in the therapeutic group and continually given for 28 days. The mean pulmonary arte-rial pressure and right ventricular hypertrophy index (RVHI), percentage of wall thickness (WT%) and percentage of wall area (WA%) of pulmonary arterioles were evaluated at day 28. The expression ofα-SMA mRNA and protein in the lung tissue were detected by Real-time PCR and Western blot. Results Mean pulmonary arterial pressure, RVHI, WT%and WA%were signiif-cantly higher in the model group than those in the therapeutic group (P<0.01) but these data in the therapeutic group were higher than that in the control group (P<0.01). The expression ofα-SMA mRNA and protein were higher in the model group than those in the control group and the therapeutic group (P<0.01), while there was no difference was found between the therapeutic group and the control group (P>0.05). Conclusions ATRA has therapeutic effect on pulmonary hypertension through down-regulation ofα-SMA expression.
