中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2009年
12期
2385-2389
,共5页
梁亚鹏%任国庆%赵高峰%王新%张超
樑亞鵬%任國慶%趙高峰%王新%張超
량아붕%임국경%조고봉%왕신%장초
血管内皮生长因子%肝素%低氧%肺动脉高压%大鼠
血管內皮生長因子%肝素%低氧%肺動脈高壓%大鼠
혈관내피생장인자%간소%저양%폐동맥고압%대서
Vascular endothelial growth factors%Heparin%Hypoxia%Pulmonary hypertension%Rats
目的:观察肝素抑制大鼠低氧性肺动脉高压过程中,血管内皮生长因子1(VEGF-1)在肺小动脉血管内皮细胞和肺组织中的表达变化.方法:成年雄性SD大鼠24只,随机分为对照组(A组)、低氧4周组(B组)和低氧+肝素4周组(C组),每组8只.测各组大鼠平均肺动脉压(mPAP)、右室肥大指数(RVHI)和血管形态学指标;HE染色观察肺动脉血管形态学改变,免疫组化法检测肺动脉血管内皮细胞VEGF-1蛋白表达;RT-PCR检测肺组织VEGF-1基因表达.结果:mPAP、RVHI、肺小动脉重塑指标、肺小动脉血管内皮细胞VEGF-1蛋白表达和肺组织VEGF-1基因表达水平在C组高于A组,低于B组.相关分析表明,VEGF-1蛋白表达与肺血管重塑呈正相关(r=0.974,P<0.01).VEGF-1mRNA与VEGF-1蛋白呈正相关(VEGF120 mRNA,r=0.919, P<0.01;VEGF164 mRNA,r=0.896, P<0.01).结论:肝素可能在转录和翻译水平抑制VEGF-1的表达,从而抑制大鼠低氧性肺动脉高压的形成.
目的:觀察肝素抑製大鼠低氧性肺動脈高壓過程中,血管內皮生長因子1(VEGF-1)在肺小動脈血管內皮細胞和肺組織中的錶達變化.方法:成年雄性SD大鼠24隻,隨機分為對照組(A組)、低氧4週組(B組)和低氧+肝素4週組(C組),每組8隻.測各組大鼠平均肺動脈壓(mPAP)、右室肥大指數(RVHI)和血管形態學指標;HE染色觀察肺動脈血管形態學改變,免疫組化法檢測肺動脈血管內皮細胞VEGF-1蛋白錶達;RT-PCR檢測肺組織VEGF-1基因錶達.結果:mPAP、RVHI、肺小動脈重塑指標、肺小動脈血管內皮細胞VEGF-1蛋白錶達和肺組織VEGF-1基因錶達水平在C組高于A組,低于B組.相關分析錶明,VEGF-1蛋白錶達與肺血管重塑呈正相關(r=0.974,P<0.01).VEGF-1mRNA與VEGF-1蛋白呈正相關(VEGF120 mRNA,r=0.919, P<0.01;VEGF164 mRNA,r=0.896, P<0.01).結論:肝素可能在轉錄和翻譯水平抑製VEGF-1的錶達,從而抑製大鼠低氧性肺動脈高壓的形成.
목적:관찰간소억제대서저양성폐동맥고압과정중,혈관내피생장인자1(VEGF-1)재폐소동맥혈관내피세포화폐조직중적표체변화.방법:성년웅성SD대서24지,수궤분위대조조(A조)、저양4주조(B조)화저양+간소4주조(C조),매조8지.측각조대서평균폐동맥압(mPAP)、우실비대지수(RVHI)화혈관형태학지표;HE염색관찰폐동맥혈관형태학개변,면역조화법검측폐동맥혈관내피세포VEGF-1단백표체;RT-PCR검측폐조직VEGF-1기인표체.결과:mPAP、RVHI、폐소동맥중소지표、폐소동맥혈관내피세포VEGF-1단백표체화폐조직VEGF-1기인표체수평재C조고우A조,저우B조.상관분석표명,VEGF-1단백표체여폐혈관중소정정상관(r=0.974,P<0.01).VEGF-1mRNA여VEGF-1단백정정상관(VEGF120 mRNA,r=0.919, P<0.01;VEGF164 mRNA,r=0.896, P<0.01).결론:간소가능재전록화번역수평억제VEGF-1적표체,종이억제대서저양성폐동맥고압적형성.
AIM: To observe the protein expression of vascular endothelial growth factor 1 (VEGF-1) in pulmonary arterial endothelial cells and VEGF-1 gene expression in lung tissue in rats with hypoxia-induced pulmonary hypertension and treated with heparin. METHODS: Twenty four male adult SD rats were randomly divided into three groups (8 rats each): a control group (group A), a group with hypoxia for 4 weeks (group B) and a group with hypoxia for 4 weeks and injected with heparin to abdominal cavity simultaneously (group C). Mean pulmonary arterial pressure (mPAP), right ventricle hypertrophy index (RVHI) and vessel morphometry were measured. The morphology of pulmonary artery was observed by HE staining. The expression of VEGF-1 protein in pulmonary arterial endothelial cells was determined by immunohistochemistry. The level of VEGF-1 mRNA in lung tissue was measured by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: mPAP, RVHI, pulmonary artery remodeling parameters, VEGF-1 protein expression in pulmonary arterial endothelial cells and VEGF-1 gene expression in lung tissue of the three groups from high to low were group B, group C and group A. It was statistically significant when compared between either two groups of the three (P<0.01). Linear correlation analysis showed that VEGF-1 protein was positively correlated with pulmonary artery remodeling parameters (r=0.974, P<0.01), and VEGF-1 mRNA was positively correlated with VEGF-1 protein (VEGF 120 mRNA, r=0.919, P<0.01; VEGF164 mRNA, r=0.896, P<0.01). CONCLUSION: Heparin may down-regulate the expression of VEGF-1 at the levels of transcription and translation, resulting in the inhibitory effect on rats with hypoxia-induced pulmonary hypertension.