Abstract：ObjectiveTo explore the effects of third-hand smoke on the level of endothelial progenitor cells (EPCs) in mice and its possible mechanism. Methods Forty 8-week-old male mice of clean grade were divided into three groups, control group(n=10, exposed to normal air), first-hand smoke group (n=15, exposed to cigarette smoke, 8 hours a day) and third-hand smoke group(n=15, exposed to sterilized dressing which had been exposed to cigarette smoke for 8 hours, 8 hours a day). Two months later, blood was collected and the levels of EPCs, myeloperoxidase (MPO), interleukin -6 (IL-6), tumor necrosis factor -α (TNF-α) and nitric oxide (NO) were measured and compared . Myocardial histological changes were observed by light microscopy. ResultsCompared with the control group, the EPC level was significantly decreased in the first-hand smoke group and the third-hand smoke group ((0.045±0.029)% vs (0.099±0.023) % and (0.047±0.023)% vs (0.099±0.023) % respectively,both P<0.001). The levels of MPO, IL-6 and TNF-α were significantly increased in the first-hand smoke group and the third-hand smoke group(MPO:1.39±0.26) U/g vs (0.48±0.17) U/g and(1.35±0.32) U/g vs (0.48±0.17) U/g;IL-6:(3.83±0.13) ng/ml vs (0.79±0.12) ng/ml and (3.45±0.15) ng/ml vs (0.79±0.12) ng/ml;TNF-α:(1.77±0.26) ng/ml vs (0.81±0.21) ng/ml and (1.78±0.23) ng/ml vs (0.81±0.21) ng/ml, all P<0.001), while the NO level was significantly decreased ((0.057±0.0063) μmol/L vs (0.080±0.0067) μmol/L and (0.060±0.0072) μmol/L vs (0.080±0.0067) μmol/L,both P<0.001). The levels of EPC, MPO, IL-6 and TNF-α were not significantly different between the first-hand smoke group and the third-hand smoke group (all P>0.05). The light microscopy indicated that the mice in the first-hand smoke group and the third-hand smoke group had obvious pathological changes in myocardial tissue. ConclusionsThird-hand smoke can reduce endothelial progenitor cell level and damage the myocardial tissue in mice by oxidative stress and inflammation. Its effects are similar with that of the first-hand smoke.
魏科华, 魏岚萍, 秦锡娟, 魏志强, 毛雪, 李娜. 三手烟对小鼠内皮祖细胞水平的影响及可能机制[J]. 实用预防医学, 2016, 23(3): 305-308.
WEI Ke-hua, WEI Lan-ping, QIN Xi-juan, WEI Zhi-qiang, MAO Xue, LI Na. Effect of third-hand smoke on the level of endothelial progenitor cells in mice and its possible mechanisms. , 2016, 23(3): 305-308.
[1] Hibbert B, Simard T, Ramirez FD, et al. The effect of statins on circulating endothelial progenitor cells in humans: a systematic review[J]. J Cardiovasc Pharmacol, 2013,62(5): 491-496. [2] Tan H, Li X, Chen W, et al. Effects of losartan on the mobilization of endothelial progenitor cells and improvement of endothelial function[J]. Ann Clin Lab Sci, 2013, 43(4): 402-406. [3] Samet JM. Tobacco smoking: the leading cause of preventable disease worldwide[J]. Thorac Surg Clin , 2013, 23(2): 103-112. [4] King BA, Mirza SA, Babb SD. A cross-country comparison of secondhand smoke exposure among adults: findings from the Global Adult Tobacco Survey (GATS) [J]. Tob Control, 2013, 22(4): e5. [5] Oberg M, Jaakkola MS, Woodward A, et al. Worldwide burden of disease from exposure to second-hand smoke: a retrospective analysis of data from 192 countries[J]. Lancet, 2011, 377(9760): 139-146. [6] Peinemann F, Moebus S, Dragano N, et al. Secondhand smoke exposure and coronary artery calcification among nonsmoking participants of a population-based cohort[J]. Environ Health Perspect, 2011, 119(11): 1556-1561. [7] Barua RS, Ambrose JA. Mechanisms of coronary thrombosis in cigarette smoke exposure[J]. Arterioscler Thromb Vasc Biol, 2013, 33(7): 1460-1467. [8] Szpak D, Grochowalski A, Chrzaszcz R, et al. Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease[J]. Pol Arch Med Wewn, 2013, 123(9): 474-481. [9] Deb A, Patterson C. Hard luck stories: the reality of endothelial progenitor cells continues to fall short of the promise[J], Circulation, 2010, 121(7): 850-852. [10] Sen S, McDonald SP, Coates PT, et al. Endothelial progenitor cells: novel biomarker and promising cell therapy for cardiovascular disease[J]. Clin Sci (Lond), 2011,120(7): 263-283.
2016, Vol. 23 
