摘要
目的:研究二氯化钴(CoC l2)诱发化学缺氧对培养的人脐静脉内皮细胞血红素氧合酶表达及增殖的影响。方法:采用MTT和流式细胞术检测人脐静脉内皮细胞的增殖,酶联免疫吸收法测定培养上清液中的碳氧血红蛋白(COHb),并通过RT-PCR观测CoC l2与血红素氧合酶表达间的量-效和时-效关系。结果:CoC l2可诱导人脐静脉内皮细胞中血红素氧合酶-1的表达,促进内源性一氧化碳(CO)的产生,与血红素氧合酶表达间有一定的剂量和时间依赖性。结论:CoC l2诱导慢性缺氧促进人脐静脉内皮细胞增殖并上调血红素氧合酶-1和内源性CO,HO/CO系统是保护内皮损伤的分子学基础,可能在妊娠期高血压疾病发病中起重要作用。
Objective：To study the effect of CoC12 induced hypoxia on the expression of hemeoxygenase and proliferation of cultural human umbilical vein endothelial cell （HUVEC）. Methods：HUVEC was cultured in vitro, the relative .amount of CO released into the media was quantitated as caron monoxide hemoglobin （COHb）by enzyme-link immunosorbent assay. Flow cymotery and MTT were performed to evaluate the effect of cell proliferation. The time-concentration relationship and time effect relationship between CoCl2 and the expression of HO-1 mRNA were explored by using reverse transcription polymerase chain reaction （RT-PCR） . Re- sults ： Proliferation of HUVEC and endogenous CO were increased significantly by CoCl2 simulated hypoxia. CoCl2 upregnlate the expression of hemeoxygenase in human umbilical vein endothelial cell in a time dependent and dose dependent manner. Conclusion： Hemeoxygenase-1 may have a protective effect on endothelial cells, the change of HO-1 mRNA, e and the HUVEC proliferation is the molecular basis of the antiapoptosis of endothelial cell. The HO-CO system may play an important role in the development of hypertensive disorder complicating pregnancy.
出处
《现代妇产科进展》
CSCD
北大核心
2006年第3期212-214,218,共4页
Progress in Obstetrics and Gynecology
关键词
二氯化钴
低氧
血红素氧合酶
人脐静脉内皮细胞
妊娠并发症
心血管
高血压
CoCl2
Hypoxia
Hemeoxygenase
Human umbilical vein endothelial cell
Pregnancy complications, cardiovascular
Hypertension
