Abstract

Background: Smoking is one of the top three causes of cardiovascular disease (CVD). Natural antioxidants including black cumin ( Nigella sativa) may inhibit the pathogenesis of initial process of atherosclerosis. The aim of this study was to determine the effect of black cumin (Nigella sativa) in preventing endothelial dysfunction mainly through macrophage M1/M2 inflammatory response in cigarette smoked male Wistars. Methods: In total, 50 Wistar rats were randomly allocated to five experimental groups: two control groups, namely no intervention (K-) and exposure to smoke of 40 cigarettes each day (K+); and three treatment groups: rats given a dose of 0.3 g (P1), 0.6 g (P2) or 1.2 g (P3) black cumin per kilograms bodyweight/ day, respectively, and exposed to smoke of 40 cigarettes each day. After 28 days of cigarette smoke exposure, macrophage M1/M2 ratio was evaluated by counting total M1 and M2 in ten microscope field of view. Data were analysed by Mann-Whitney test. Results: The M1 / ​​M2 ratio on K (-) was0.97 ±0.98 (<1) which means M2 was dominant,while the M1 / ​​M2 ratio on K (+)was of4.97 ± 3.42(> 1) which means M1 dominant.There was no significant difference in the number of M1 count in treatment groups P1, P2, P3 (p value =0.996; 0.170;0.884, respectively) when compared with K+.Additionally, P2 group has the lower M1 number with the highest significance value when compared to K+.The number of M1 counts on P1 did not differ significantly when compared to P2 withp= 0.121 and P3 with p =0.936. Conclusions: In sum, ethanol extract of black cumin prevents endothelial dysfunction by inhibiting increase in macrophages M1 / M2 ratioinrats Wistar exposed to sub-chronic cigarette smoke.

Highlights

  • Endothelial dysfunction is a leading predictor for atherosclerotic development and coronary heart disease (CHD).[1,2] Atherosclerosis is a disease of the blood vessel wall caused by the accumulation of lipids and fibrous tissue in blood vessels, progressively narrowing the lumen of blood vessels.[3]

  • Endothelial dysfunction is characterized by a decrease in the endhotelial nitrite oxide synthase enzyme due to oxidative stress. eNOS affects the bioavailability of nitric oxide (NO) which results in decreased antioxidant, anti-inflammatory and anti-thrombotic activity in blood vessels

  • Nitric oxide is mainly produced by the assistance of endothelial nitric oxide synthase (e-NOS)

Read more

Summary

Introduction

Endothelial dysfunction is a leading predictor for atherosclerotic development and coronary heart disease (CHD).[1,2] Atherosclerosis is a disease of the blood vessel wall caused by the accumulation of lipids and fibrous tissue in blood vessels, progressively narrowing the lumen of blood vessels.[3]. Global data shows that smoking, including second-hand smoke, is one of the top three causes of heart disease in the world and contributed to 7.2 million deaths in 2015.4 Law and Wald (2003) evaluated the association between smoking and CHD which shows a positive correlation between the number of cigarettes smoked per day and relative risk of CHD.[5,6] Cigarettes contain seven thousand kinds of chemicals that narrow the arteries and damage the blood vessels which leads to endothelial dysfunction.[7]. The aim of this study was to determine the effect of black cumin (Nigella sativa) in preventing endothelial dysfunction mainly through macrophage M1/M2 inflammatory response in cigarette smoked male Wistars. Conclusions: In sum, ethanol extract of black cumin prevents endothelial dysfunction by inhibiting increase in macrophages M1 / M2 ratio in rats Wistar exposed to sub-chronic cigarette smoke

Objectives
Methods
Findings
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.