缺氧时猪肺动脉平滑肌细胞中环氧合酶和血栓素合酶基因表达变化研究  

The Expression of Cycloxygenase and Thromboxane Synthase Genes in Smooth Muscle Cells during Hypoxia

作　　者：于江洲[1] 王迪浔[1] 

机构地区：[1]同济医科大学基础医学院病理生理学教研室,武汉430030

出　　处：《同济医科大学学报》1997年第1期7-9,共3页Acta Universitatis Medicinae Tongji

基　　金：国家"八五"攻关项目!85-915-03-06

摘　　要：应用培养的猪肺动脉平滑肌细胞经分子杂交和放射免疫检测发现:缺氧可使环氧合酶（COX）基因表达增加，缺氧6、24、48h，环氧合酶-2（COX-2）和环氧合酶-1（COX-1）mRNA水平分别是常氧组的3、1、1倍和1、2、2.7倍。并在不同时间缺氧（6、24、48h），平滑肌细胞条件培养基中6-酮-前列腺素Flα含量也显著高于相应对照组（P＜0.05），但缺氧对血栓素合酶（TXS）基因表达及血栓素入生成无明显影响。结果表明:缺氧可使平滑肌细胞COX基因表达及前列环素（PGI2）自分泌增加，它可能在平滑肌细胞缺氧收缩及增生反应中起调节作用。并且从缺氧时COX和PGI2生成的动态变化说明，缺氧时PGI2生成的迅速增多主要与COX-2mRNA表达增加有关。By using molecular hybridization and radio immunoassay, it was found that hypoxia increased the COX gene expression in porcine pulmonary artery smooth muscle cells (PASMCs), that when exposed to hypoxia for 6, 24 and 48 hours, the COX-1 and COX-2 mRNA levels were 1, 2 and 2. 7 times and 3, 1 and 1 times compared with normoxic group, respectivly, and that the content of 6-Keto-PGFla in conditioned cultured medium of PASMCs in hypoxia was elevated significantly in comparision with normoxic groups (P＜0.05). However, hypoxia didn't affect the TXS gene expression and TXA2 production in PASMCs. Our results show that hypoxia may promote the COX gene expression and PGI2 production, which might play a role in regulating smooth muscle cells contraction and proliferation in hypoxia and that the increase of COX-2 gene expression might mainly contribute to the earlier production of PGI2 by PASMCs in hypoxia.

关 键 词：肺动脉 缺氧症 环氧水合酶 血栓素合酶 基因表达 

分 类 号：R594.3[医药卫生—内科学] R364.4[医药卫生—临床医学]