Boldine reduces left ventricle oxidative stress in isoproterenol-induced adrenergic overload experimental model.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-12-22 DOI:10.1080/13813455.2024.2441363

Elissa Kerli Fernandes, Patrick Türck, Cristina Campos Carraro, Silvio Tasca, Isabel Cristina Teixeira Proença, Victor De Mello Palma, Fernanda Visioli, Iraci Lucena Da Silva Torres, Adriane Belló-Klein, Alexandre Luz De Castro, Alex Sander Da Rosa Araujo

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Abstract

Sustained adrenergic overload in the heart causes maladaptive cardiac remodelling, which involves oxidative stress. Boldine (BOL) has antioxidant activity and represents a novel therapeutic approach. This study explored the cardioprotective role of BOL in adverse left ventricular remodelling induced by isoproterenol. The rats were divided into four groups: control; BOL (25 mg/kg daily); isoproterenol (ISO) (5 mg/kg daily), and ISO + BOL. Morphometric, echocardiographic, and oxidative stress parameters were evaluated. BOL attenuated both cardiac hypertrophy and increased diastolic volume caused by adrenergic overstimulation (P < 0.05). BOL treatment reduced lipid peroxidation induced by ISO (ISO vs. ISO + BOL; P < 0.05), and this effect was associated with increased superoxide dismutase (SOD) (ISO vs. ISO + BOL; P < 0.05) and glutathione-S-transferase levels (GST) (ISO vs. ISO + BOL; P < 0.05). This data suggest that BOL may improve cardiac oxidative stress and attenuate some parameters of adverse cardiac remodelling.

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Boldine降低异丙肾上腺素诱导的肾上腺素能过载实验模型左心室氧化应激。

心脏持续的肾上腺素能超负荷导致心脏重构不适应，这涉及氧化应激。Boldine （BOL）具有抗氧化活性，是一种新的治疗方法。本研究探讨了BOL在异丙肾上腺素诱导的不良左心室重构中的心脏保护作用。将大鼠分为四组：对照组；BOL（每日25毫克/公斤）；异丙肾上腺素（ISO）（每天5mg /kg）和ISO + BOL。评估形态学、超声心动图和氧化应激参数。BOL减轻了肾上腺素能过度刺激引起的心脏肥大和舒张容积增加(P

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.