Cigarette Smoking-Induced Cardiac Hypertrophy, Vascular Inflammation and Injury Are Attenuated by Antioxidant Supplementation in an Animal Model

Abstract

Background: Cardiovascular diseases are the leading causes of morbidity and mortality worldwide. Cigarette smoking remains a global health epidemic with associated detrimental effects on the cardiovascular system. In this work, we investigated the effects of cigarette smoke exposure on cardiovascular system in an animal model. The study then evaluated the effects of antioxidants (AO), represented by pomegranate juice, on cigarette smoke induced cardiovascular injury. This study aims at evaluating the effect of pomegranate juice supplementation on the cardiovascular system of an experimental rat model of smoke exposure.Methods: Adult rats were divided into four different groups: Control, Cigarette smoking (CS), AO, and CS + AO. Cigarette smoke exposure was for 4 weeks (5 days of exposure/week) and AO group received pomegranate juice while other groups received placebo. Assessment of cardiovascular injury was documented by assessing different parameters of cardiovascular injury mediators including: (1) cardiac hypertrophy, (2) oxidative stress, (3) expression of inflammatory markers, (4) expression of Bradykinin receptor 1 (Bdkrb1), Bradykinin receptor 2 (Bdkrb2), and (5) altered expression of fibrotic/atherogenic markers [(Fibronectin (Fn1) and leptin receptor (ObR))].Results: Data from this work demonstrated that cigarette smoke exposure induced cardiac hypertrophy, which was reduced upon administration of pomegranate in CS + AO group. Cigarette smoke exposure was associated with elevation in oxidative stress, significant increase in the expression of IL-1β, TNFα, Fn1, and ObR in rat's aorta. In addition, an increase in aortic calcification was observed after 1 month of cigarette smoke exposure. Furthermore, cigarette smoke induced a significant up regulation in Bdkrb1 expression level. Finally, pomegranate supplementation exhibited cardiovascular protection assessed by the above findings and partly contributed to ameliorating cardiac hypertrophy in cigarette smoke exposed animals.Conclusion: Findings from this work showed that cigarette smoking exposure is associated with significant cardiovascular pathology such as cardiac hypertrophy, inflammation, pro-fibrotic, and atherogenic markers and aortic calcification in an animal model as assessed 1 month post exposure. Antioxidant supplementation prevented cardiac hypertrophy and attenuated indicators of atherosclerosis markers associated with cigarette smoke exposure.

<p>Combined Effect Of Coffee Consumption And Cigarette Smoking On Serum Levels Of Vitamin B12, Folic Acid, And Lipid Profile In Young Male: A Cross-Sectional Study</p>

“…Accordingly, our findings may refer to a potential absorptive effect of cigarette smoking and/or moderate coffee consumption (MCC) on the negative consequences of excessive consumption of coffee as shown in the combined effect of both factors by the results of two-way ANOVA test. However, hyperlipidemic levels of LDL-C and TC have been correlated with the separate effect of HCC and cigarette smoking in humans 18,27,28 and animal models. [29][30][31][32] Nevertheless, some studies showed that caffeine has significant effects 11,23 or no effect on the lipid profile.…”

“…17 Correspondingly, the association of cigarette smoking with CVDs can be attributed to increased oxidative stress due to excessive free radicals resulted from burning tobacco and other chemicals of the cigarettes. 18,19 Nicotine, which is the main component of cigarette smoke, causes coronary death by provoking ventricular arrhythmias. Cardiac effects of nicotine happen due to the stimulation of nicotinic receptor, which enhances the release of catecholamine.…”

Protective Effects of Hydrogen Sulfide Against Cigarette Smoke Exposure-Induced Placental Oxidative Damage by Alleviating Redox Imbalance via Nrf2 Pathway in Rats

“…A vast array of evidence indicates that excessive ROS production, exceeding the anti-oxidative capacity of cells, may damage cell components such as DNA, protein, and lipids, and then cause cellular dysfunction [20]. Meanwhile, a number of adverse events associated with oxidative stress are observed in tissues following CSE, which include cardiac hypertrophy [21], pulmonary fibrosis [22] as well as endothelial cells injury [23]. In mammalian cells, ROS is scavenged by a host of enzymatic antioxidants including superoxide dismutase (SOD), catlase (CAT) and glutathione peroxidase (GPx), and nonenzymatic antioxidants, such as glutathione (GSH) [20,24].…”

Antiinflammatory and anti‐cancer activities of pomegranate and its constituent, ellagic acid: Evidence from cellular, animal, and clinical studies

“…In another study, the effects of pomegranate juice concentrate (equivalent to 80 μmol polyphenols/mL) were measured on cigarette smoking‐induced‐cardiac hypertrophy in rats. It has been demonstrated that pomegranate juice mitigates the ROS level, ObR, and Fn1 fibrotic markers, Bdkrb1 and Bdkrb2 kinin receptor, IL‐1β and TNF‐α expression level in aorta of rats (Al Hariri et al, ).…”

“…In another study, the effects of pomegranate juice concentrate (equivalent to 80 μmol polyphenols/mL) were measured on cigarette smoking-induced-cardiac hypertrophy in rats. It has been demonstrated that pomegranate juice mitigates the ROS level, ObR, and Fn1 fibrotic markers, Bdkrb1 and Bdkrb2 kinin receptor, IL-1β and TNF-α expression level in aorta of rats(Al Hariri et al, 2016).Cornélio Favarin et al evaluated the effects of EA (10 mg/kg; orally) in the ALI induced by spitting acid in the left lung of mice. EA attenuated the permeability of blood vessels and the number of neutrophils in BALF.…”