Protective effect of Galectin-3 inhibitor against cardiac remodelling in an isoprenaline-induced myocardial infarction in type 2 diabetes.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-08-05 DOI:10.1080/13813455.2024.2387710

Manal Moustafa Mahmoud, Mai Mohammed Hassan, Hany El-Sebaee Elsayed, Amal E Fares, Mona M Saber, Laila Ahmed Rashed, Omaima Mohammed Abdelwahed

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Abstract

Type 2 Diabetes mellitus (T2DM) has the potential to impair cardiac function and cause heart failure. We aimed to study the cardioprotective influence of Galactin-3 (Gal-3) inhibitor; modified citrus pectin (MCP) in isoprenaline induced myocardial infarction (MI) in T2DM rats. Forty rats were allocated into 4 groups; groups I and II served as control. T2DM was provoked in groups III and IV by serving them high fat diet followed by a single low dose of Streptozotocin (STZ), then group IV were administered MCP in drinking water for 6 weeks. Groups III and IV were then subcutaneously injected isoprenaline hydrochloride once daily on the last 2 successive days to induce MI. MCP restored echocardiographic parameters with significant decline in Gal-3 area % in cardiac tissue alongside protection against cardiac remodelling. our data showed that there is a protective potential for Gal-3 inhibitor (MCP) against cardiac injury in isoprenaline induced MI in T2DM.

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Galectin-3 抑制剂对异丙肾上腺素诱发的 2 型糖尿病心肌梗死心脏重构的保护作用

2 型糖尿病（T2DM）有可能损害心脏功能并导致心力衰竭。我们旨在研究半乳糖苷-3（Gal-3）抑制剂；改良柑橘果胶（MCP）对异丙肾上腺素诱发的 T2DM 大鼠心肌梗死（MI）的心脏保护作用。40 只大鼠被分为 4 组，I 组和 II 组为对照组。Ⅲ组和Ⅳ组通过高脂饮食诱发 T2DM，然后给予单次低剂量链脲佐菌素（STZ），然后给Ⅳ组大鼠在饮用水中添加 MCP，持续 6 周。然后，连续2天给III组和IV组每天皮下注射一次盐酸异丙肾上腺素，诱发心肌梗死。我们的数据表明，在异丙肾上腺素诱导的 T2DM 心肌梗死中，Gal-3 抑制剂（MCP）对心脏损伤具有保护潜力。

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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.

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