中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2014年
2期
109-112
,共4页
陈蕊%刘培晶%严金川%顾雨春
陳蕊%劉培晶%嚴金川%顧雨春
진예%류배정%엄금천%고우춘
二十二碳六烯酸%高血压,肺性%低氧
二十二碳六烯痠%高血壓,肺性%低氧
이십이탄륙희산%고혈압,폐성%저양
Docosahexaenoic acid%Hypertension,pulmonary artery%Hypoxia
目的 探讨二十二碳六烯酸(DHA)对低氧性肺动脉高压的影响及机制.方法 实验SD大鼠分为常氧组、常氧DHA组、低氧组和低氧DHA组.肺动脉高压模型采用间断低氧法,大鼠肺小动脉形态学采用HE染色,肺动脉平滑肌细胞(PASMCs)采用组织贴块法,细胞增殖及迁移分别采用噻唑蓝比色法和改良Boyden小室法.α-肌动蛋白、调宁蛋白和肌动蛋白相关蛋白(SM22α) mRNA水平采用RT-PCR法.结果 低氧组大鼠平均肺动脉压力[mPAP,(30.1±2.6) mmHg,1 mmHg=0.133 kPa],右心室肥厚指数[RV/(LV +S),(40.4±4.2)％],肺小动脉管壁厚度与外径比值[WT％,(44.6±4.1)％]及管壁面积占血管总面积的百分比[WA％,(81.2±5.4)％]与常氧对照组相比均明显升高[mPAP:(18.4±1.2) mmHg；RV/(LV+S):(27.8±1.6)％；WT％:(17.7±3.3)％;WA％:(42.9±3.5)％,P＜0.05]；DHA干预的低氧组大鼠上述各指标[mPAP为(22.7±1.8)mmHg,RV/(LV +S)为(34.2±2.2)％,WT％为(21.6±4.1)％,WA％为(52.0±2.9)％]均低于低氧组(P＜0.05)；常氧DHA组,低氧DHA组与常氧组相比,上述指标无显著差别.在体外,DHA能显著抑制低氧诱导的PASMCs增殖、迁移(P＜0.05).低氧时DHA能促进α-肌动蛋白,调宁蛋白和SM22α的mRNA表达.结论 DHA对低氧所致的肺动脉高压具有较好的抑制作用,其机制可能是通过抑制PASMCs增殖,迁移和表型转换而起作用.
目的 探討二十二碳六烯痠(DHA)對低氧性肺動脈高壓的影響及機製.方法 實驗SD大鼠分為常氧組、常氧DHA組、低氧組和低氧DHA組.肺動脈高壓模型採用間斷低氧法,大鼠肺小動脈形態學採用HE染色,肺動脈平滑肌細胞(PASMCs)採用組織貼塊法,細胞增殖及遷移分彆採用噻唑藍比色法和改良Boyden小室法.α-肌動蛋白、調寧蛋白和肌動蛋白相關蛋白(SM22α) mRNA水平採用RT-PCR法.結果 低氧組大鼠平均肺動脈壓力[mPAP,(30.1±2.6) mmHg,1 mmHg=0.133 kPa],右心室肥厚指數[RV/(LV +S),(40.4±4.2)％],肺小動脈管壁厚度與外徑比值[WT％,(44.6±4.1)％]及管壁麵積佔血管總麵積的百分比[WA％,(81.2±5.4)％]與常氧對照組相比均明顯升高[mPAP:(18.4±1.2) mmHg；RV/(LV+S):(27.8±1.6)％；WT％:(17.7±3.3)％;WA％:(42.9±3.5)％,P＜0.05]；DHA榦預的低氧組大鼠上述各指標[mPAP為(22.7±1.8)mmHg,RV/(LV +S)為(34.2±2.2)％,WT％為(21.6±4.1)％,WA％為(52.0±2.9)％]均低于低氧組(P＜0.05)；常氧DHA組,低氧DHA組與常氧組相比,上述指標無顯著差彆.在體外,DHA能顯著抑製低氧誘導的PASMCs增殖、遷移(P＜0.05).低氧時DHA能促進α-肌動蛋白,調寧蛋白和SM22α的mRNA錶達.結論 DHA對低氧所緻的肺動脈高壓具有較好的抑製作用,其機製可能是通過抑製PASMCs增殖,遷移和錶型轉換而起作用.
목적 탐토이십이탄륙희산(DHA)대저양성폐동맥고압적영향급궤제.방법 실험SD대서분위상양조、상양DHA조、저양조화저양DHA조.폐동맥고압모형채용간단저양법,대서폐소동맥형태학채용HE염색,폐동맥평활기세포(PASMCs)채용조직첩괴법,세포증식급천이분별채용새서람비색법화개량Boyden소실법.α-기동단백、조저단백화기동단백상관단백(SM22α) mRNA수평채용RT-PCR법.결과 저양조대서평균폐동맥압력[mPAP,(30.1±2.6) mmHg,1 mmHg=0.133 kPa],우심실비후지수[RV/(LV +S),(40.4±4.2)％],폐소동맥관벽후도여외경비치[WT％,(44.6±4.1)％]급관벽면적점혈관총면적적백분비[WA％,(81.2±5.4)％]여상양대조조상비균명현승고[mPAP:(18.4±1.2) mmHg；RV/(LV+S):(27.8±1.6)％；WT％:(17.7±3.3)％;WA％:(42.9±3.5)％,P＜0.05]；DHA간예적저양조대서상술각지표[mPAP위(22.7±1.8)mmHg,RV/(LV +S)위(34.2±2.2)％,WT％위(21.6±4.1)％,WA％위(52.0±2.9)％]균저우저양조(P＜0.05)；상양DHA조,저양DHA조여상양조상비,상술지표무현저차별.재체외,DHA능현저억제저양유도적PASMCs증식、천이(P＜0.05).저양시DHA능촉진α-기동단백,조저단백화SM22α적mRNA표체.결론 DHA대저양소치적폐동맥고압구유교호적억제작용,기궤제가능시통과억제PASMCs증식,천이화표형전환이기작용.
Objective To investigate the effects of docosahexaenoic acid (DHA) on hypoxiainduced pulmonary arterial hypertension (PAH) and the mechanism.Methods PAH was induced by chronic intermittent hypoxia for 21 days in vivo.Forty male Sprague-Dawley rats were randomly divided into 4 groups (n =10,each):a normal control group,DHA-treated groups in normoxia and hypoxia,and a PAH group.At the end of study,mean pulmonary arterial pressure (mPAP),right ventricular hypertrophy and the index of wall thickness of small pulmonary artery (WT％ and WA％) among groups were compared.The changes of pulmonary arterial smooth muscle cell (PASMC) proliferation were determined by MTT in vitro.Migration assay was performed using the Boyden chamber.Real-time quantitative PCR was performed to quantify mRNA levels of the smooth muscle cell phenotype markers SM-α-actin,calponin and SM 22α under normoxic or hypoxic conditions,in the absence or presence of DHA.Results DHA treatment significantly lowered mPAP[(22.7 ± 1.8) mmHg (1 mmHg =0.133 kPa)],reduced thickening of small pulmonary artery wall[WT％:(21.6 ± 4.1) ％,WA％:(52.0 ± 2.9) ％] and alleviated ventricular hypertrophy (34.2 ± 2.2) ％ compared to those of the hypoxic group (P ＜ 0.05).DHA inhibited the proliferation,migration and phenotype switching of PASMCs induced by hypoxia in vitro.Conclusion DHA therapy reduced mPAP in a rat model of hypoxia-induced PAH and this effect was linked with inhibition of pulmonary vascular remodelling.
