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Archives of Physiology and Biochemistry
The Journal of Metabolic Diseases
Volume 129, 2023 - Issue 4
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Original Articles

N-acetyl cysteine can blunt metabolic and cardiovascular effects via down-regulation of cardiotrophin-1 in rat model of fructose-induced metabolic syndrome

ORCID Icon, , &
Pages 854-869 | Received 17 Aug 2020, Accepted 08 Jan 2021, Published online: 28 Jan 2021
 

Abstract

In this study, we investigated the ability of N-acetyl cysteine (NAC) to alleviate the metabolic disorders in fructose-induced metabolic syndrome (MS) in male rats and to examine its protective effect on aortic and cardiac tissues via its influence on cardiotrophin-1 (CT-1) expression. NAC (20 mg/kg b.w./day) was administered to fructose induced MS animals for 12 weeks. Chronic fructose consumption (20% w/v) increased body weight gain, relative heart weight, systolic blood pressure (SBP), diastolic blood pressure (DBP), insulin resistance (IR), and associated with metabolic alterations. Histological and immunohistochemical examination revealed aortic stiffness and myocardial degeneration and fibrosis together with increased CT-1 expression. Treatment with NAC improved IR, SBP, DBP, and mitigated dyslipidaemia and oxidative stress. Additionally, NAC down-regulated CT-1 expression in the heart and aorta. These findings demonstrated the protective effect of NAC against aortic and myocardial degeneration and fibrosis through down-regulation of CT-1 in fructose induced MS animal model.

Author contributions

All authors conceived and planned the experiments. A.S.A. and M.B.T. carried out the experiment and statistical analysis. A.S.A. wrote the manuscript with support from E.A.A. A.M.A. performed the histopathological and immunohistochemistry part of the study. All authors discussed the results and commented on the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The datasets used and analysed during the current study available from the corresponding author on reasonable request.

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