Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke.

Maria Angélica Martins Lourenço,Leonardo Antonio Mamede Zornoff,Ana Angélica Henrique Fernandes,Marcos Ferreira Minicucci,Paula Schmidt Azevedo,Renata Aparecida Cândido Da Silva,Bertha Furlan Polegato,Tatiana Fernanda Bachiega,Silmeia Garcia Zanati,Mariana Gobbo Braz,Sergio Alberto Rupp De Paiva,Aline Garcia Aun,Amanda Menezes Figueiredo,Patrícia Helena Correa Alegre,Elisa Moya Kazmarek,Bruna Letícia Buzati Pereira

doi:10.1111/jcmm.13683

Maria Angélica Martins Lourenço, Leonardo Antonio Mamede Zornoff + Show 14 more

Open Access

https://doi.org/10.1111/jcmm.13683

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Abstract

The objective of this study was to investigate the influence of Spondias mombin (SM) supplementation on the cardiac remodelling process induced by exposure to tobacco smoke (ETS) in rats. Male Wistar rats were divided into 4 groups: group C (control, n = 20) comprised animals not exposed to cigarette smoke and received standard chow; group ETS (n = 20) comprised animals exposed to cigarette smoke and received standard chow; group ETS100 (n = 20) received standard chow supplemented with 100 mg/kg body weight/d of SM; and group ETS250 (n = 20) received standard chow supplemented with 250 mg/kg body weight/d of SM. The observation period was 2 months. The ETS animals had higher values of left cardiac chamber diameters and of left ventricular mass index. SM supplementation attenuated these changes. In addition, the myocyte cross‐sectional area (CSA) was lower in group C compared with the ETS groups; however, the ETS250 group had lower values of CSA compared with the ETS group. The ETS group also showed higher cardiac levels of lipid hydroperoxide (LH) compared with group C; and, groups ETS100 and ETS250 had lower concentrations of LH compared with the ETS group. Regarding energy metabolism, SM supplementation decreased glycolysis and increased the β‐oxidation and the oxidative phosphorylation. There were no differences in the expression of Nrf‐2, SIRT‐1, NF‐κB, interferon‐gamma and interleukin 10. In conclusion, our results suggest that ETS induced the cardiac remodelling process. In addition, SM supplementation attenuated this process, along with oxidative stress reduction and energy metabolism modulation.

Highlights

Exposure to tobacco smoke is considered the most important cause of preventable death in the world.[1]
Male Wistar rats weighing 200-250 g were divided into 4 groups: group C comprised animals not exposed to cigarette smoke and received standard chow; group exposure to tobacco smoke (ETS) comprised animals exposed to cigarette smoke and received standard chow; group ETS100 (n = 20) animals were exposed to cigarette smoke and received standard chow supplemented with 100 mg/kg body weight/d of Spondias mombin (SM); and group ETS250 (n = 20) animals were exposed to cigarette smoke and received standard chow supplemented with 250 mg/ kg body weight/d of SM.[25]
There was no difference among body weights in the beginning of the study; the groups exposed to cigarette smoke had lower body weight at the end of the experiment compared with the control group (Table 1)

Summary

Introduction

Exposure to tobacco smoke is considered the most important cause of preventable death in the world.[1]. According to Cohn et al,[12] the cardiac remodelling may be defined as genome expression, molecular, cellular and interstitial changes that are manifested clinically as changes in size, shape and function of the heart after cardiac injury. In the acute phase of cardiac injury, remodelling is an adaptive process enabling the heart to maintain function; chronically it leads to heart failure and death.[12]

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