Aim Despite its increasing popularity, little is well known about the health effects of waterpipe smoking (WPS), particularly on the cardiovascular system
February 19, 2021
Aim Despite its increasing popularity, little is well known about the health effects of waterpipe smoking (WPS), particularly on the cardiovascular system. induced inflammation by studying the effect of WPS on the content and activity of AMPK, eNOS proteins and NF-B p65 ser536 phosphorylation, respectively. WSC inhibited AMPK/eNOS phosphorylation and induced phosphorylation of p65. Moreover, we evaluated endothelial cells repair mechanism related properties that include migration/invasion and in vitro pipe development upon treatment with WSC. WSC decreased the GSK467 motility and inhibited angiogenic potential of HAEC cells. Conclusions WPS induced endothelial cell dysfunction as apparent by exerting oxidative tension, inflammation, and impaired endothelial vasodilatory restoration and function systems. Altogether these data provide evidence for the potential contribution of WPS to endothelial dysfunction and thus to vascular disease. tobacco mixture with that of a single cigarette, Shihadeh showed that waterpipe smokers are exposed to substantial amounts of nicotine, CO, tar, polycyclic aromatic hydrocarbons and heavy metals such as arsenic, cobalt, chromium, and lead (Al Rashidi et al., 2008; Shihadeh and Saleh, 2005). The data suggest that, relative to a single cigarette, a single waterpipe smoking session is associated with 1.7 times the nicotine, 6.5 times the CO, and 46.4 times the tar (Djordjevic et al., 2000; Shihadeh and Saleh, 2005). These results indicate that waterpipe smoke condensate (WSC) contains alarming levels of toxicants know as causal factors in the initiation and elevated incidence of cardiovascular disease (CVD) in cigarette smokers (Ambrose and Barua, 2004). Since the adverse effects of cigarette smoke have been thoroughly documented in relation to CVD and because many toxic constituents of WSC overlap with or exceed that of cigarette smoke, therefore, more research is needed to clarify waterpipe-induced risk of tobacco-caused diseases, particularly CVD. A few studies (AKl et al., 2010; Neergaard et al., 2007) addressing the adverse health consequences of WPS show an association with a variety of health risks similar to those associated with cigarette smoking. Of particular interest is the finding that WPS is as important risk factor as cigarette smoking for CVD with WPS associated with increased risk of atherosclerosis (Israel et al., 2003) and coronary heart disease (Jabbour et al., 2003). Recent studies by Wolfram et al. also exhibited that WPS exerts a significant pro-oxidant atherogenic stimulus (Wolfram et al., 2003). By measuring 8-epi-PGF2a levels, a marker for in vivo oxidation injury, Wolfram et al. showed significant increase in 8-epi-PGF2a levels in waterpipe smokers that was also elevated in cigarette smokers. Furthermore, two studies assessing the acute effects of WPS on some parameters of the cardio-respiratory system detected acute biologic GSK467 changes that might result in health problems (Hakim et al., 2011; Shaikh et al., 2008). Recent studies on human subjects exhibited significant elevation of blood pressure and heart rate observed among waterpipe smokers (Al-Kubati GSK467 et al., 2006; Al-Safi, 2005; Shafagoj and Mohammed, 2002). The endothelium is the second site to encounter the products of tobacco combustion (Blann and McCollum, 1993) and its dysfunction is an early feature of atherogenesis in vitro (Celermajer et al., 1996). The endothelium is an active, dynamic tissue that controls many important functions. It plays a vital role in vascular homeostasis, vascular tone regulation, thrombosis, angiogenesis, and inflammation (Fltou, 2011). In response to various stimuli, endothelial cells produce and release a large number of vasoactive substances, growth modulators and other factors that mediate these functions. However, cardiovascular risk factors, like smoking, alter many of the normal endothelial functions which precede the development of pathological changes and subsequent clinical complications (Reriani et al., 2010). In Rabbit Polyclonal to MOBKL2B this study, we investigate the effect of mainstream WSC on endothelial cell function in vitro and discuss the implication of these cellular responses in the pathophysiology of vascular disease. 2. Materials and methods 2.1. Smoking machine protocol.