野生型p53、bcl_2基因在低氧性肺动脉高压大鼠肺内表达及其分布  

EXPRESSION AND DISTRIBUTION OF p53 AND BCL_2 IN THE LUNG TISSUE OF RATS WITH CHRONIC HYPOXIC PULMONARY HYPERTENSION

作　　者：李荣[1] 别毕华[1] 彭则[1] 张珍祥[1] 

机构地区：[1]同济医科大学附属同济医院呼吸病研究室,武汉430030

出　　处：《中国应用生理学杂志》2000年第3期246-249,共4页Chinese Journal of Applied Physiology

摘　　要：目的 :探讨野生型 p5 3、bcl2 基因在慢性低氧性肺动脉高压中的作用。方法 :建立慢性低氧性肺动脉高压大鼠模型 ,用原位杂交的方法观察 p5 3mRNA、bcl2 mRNA在大鼠心脏及肺组织的表达和分布。结果 :缺氧组大鼠肺小动脉壁厚度占血管外径的百分比 (MT % ) 2 9 3 %± 4 5 %明显高于正常对照组 15 2 %± 3 2 % (P <0 .0 1) ,肺小动脉壁 p5 3mRNA表达 0 6 8± 0 12明显弱于对照组 1 12± 0 38(P <0 .0 1) ,而bcl2 mRNA表达 2 38± 1 0 4强于对照组 1 0 9± 0 32 (P <0 .0 1)。结论 :①慢性缺氧能导致肺小动脉重建及肺动脉高压 ;②野生型 p5 3bcl2 基因均参与了慢性低氧性肺动脉高压肺血管重建的调控。Aim:To evaluate the role of p53 and bcl 2 in the development of hypoxic pulmonary hypertension.Methods:Rat models with chronic hypoxia induced pulmonary hypertension were established.Expression and distrbution of p53 mRNA and bcl 2 mRNA in the rat lung tissue and heart were detected with in situ hybridization.Results:The ratio of the thickness of pulmonary arteriolar wall to external diameter of pulmonary arterioles (MT%) was (29.3%±4.5%)in rats exposed to hypoxia for 3 weeks.It was significantly higher than those in normal control group (15.2%±3.2, P <0.01).The expression of p53 mRNA in the wall of pulmonary arterioles in hypoxic rats was weaker (0.68±0.12) than that of control group (1.12±0.38, P <0.01),but the expression of bcl 2 mRNA in the wall of pulmonary arterioles in hypoxic rats was stronger (2.38±1.04) than that of control group (1.09±0.32, P <0.01).Conclusion:①Hypoxia can induce formation of pulmonary hypertension and structural reure remodeling of pulmonary arteriols in chronic hypoxic pulmonary hypertension.②p53 and bcl 2 amy modulate the structure remodeling of pulmomary arterioles in chronic hypoxic pulmonary hypertension.

关 键 词：缺氧 高血压 肺 BCL2 P53 

分 类 号：R543.2[医药卫生—心血管疾病] Q786[医药卫生—内科学]