Damaging Effect of Cigarette Smoke Extract on PrimaryCultured Human Umbilical Vein Endothelial Cells and Its Mechanism  

作　　者：Yu-MEIYANG GENG-TAOLIU 

机构地区：[1]DivisionofPharmacology,InstituteofMateriaMedica,ChineseAcademyofMedicalSciences,PekingUnionMedicalCollege,1XianNongTanStreet,Beijing100050,China

出　　处：《Biomedical and Environmental Sciences》2004年第2期121-134,共14页生物医学与环境科学（英文版）

摘　　要：Objective To investigate the cellular effects of cigarette smoke extract (CSE) on primarily cultured human umbilical vein endothelial cells (HUVEC). Methods The effects of CSE (5%-20%) and nicotine (10-4 mol/L) on HUVEC viability, proliferation, angiogenesis and apoptosis were observed. Results CSE decreased HUVEC survival rate and angiogenesis after 24 h as well as its proliferation after 48 h in a dose-dependent manner. Moreover, CSE induced apoptosis of HUVEC as indicated in condensation of nuclear chromatin and the presence of hypodiploid DNA. HUVEC incubated with CSE for 24 h gave a significant decrease in the expression of Bcl-2 as well as the decline in the Bcl-2/Bax ratio accompanied with the loss of mitochondrial membrane potential and excess cytosolic calcium. Our study also observed that p53 protein level decreased, rather than increased in cells treated with CSE. Nicotine had no discernible inhibitory effects on the above indices of HUVEC. Conclusion Exposure to CSE other than nicotine causes inhibition of viability, proliferation and differentiation of HUVEC. CSE-induced HUVEC injury is mediated in part through accelerated apoptosis but independent of p53 pathway. It appears that mitochondria have played a key role in the apoptosis of HUVEC induced by CSE.

关 键 词：Cigarette smoke extracts (CSE) Human umbilical endothelial cell (HUVEC) VIABILITY Proliferation ANGIOGENESIS Mitochondrial membrane potential Cytosolic calcium Bcl-2 BCL-2/BAX p53 

分 类 号：R163[医药卫生—公共卫生与预防医学]