酰化胃泌素保护通过抑制钙神经蛋白和激活 ARC 来抑制心肌梗死后远端心肌的细胞凋亡。

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-04-01 Epub Date: 2021-12-29 DOI:10.1080/13813455.2021.2017463

Refaat A Eid

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引用次数: 0

摘要

本研究探讨了酰化胃泌素（AG）是否能抑制雄性大鼠左心室心肌梗死（MI）诱导的细胞凋亡，并检验了这种保护作用是否涉及调节 ARC 抗凋亡蛋白。大鼠（n = 12/组）被分配为假手术、假+AG（100 µg/kg，2x/d，S.C.）、心肌梗死和心肌梗死+AG。在没有抗氧化活性或 FAS 表达的情况下，AG 可抑制 caspase-3、8 和 9，并降低假手术大鼠和 MI 处理大鼠左心室中细胞色素-c、Bax、Bad 和 Bad-BCL-2 复合物的细胞膜/线粒体水平。与此同时，AG 保护了线粒体结构，降低了 mtPTP，并增强了两个处理组大鼠左心室的状态-3 呼吸。这些作用与线粒体中 ARC 水平的增加和钙神经蛋白活性的降低有关。总之，AG 可通过抑制钙调素、激活 ARC 和保护线粒体完整性来抑制 MI 诱导的心室凋亡。

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Acylated ghrelin protection inhibits apoptosis in the remote myocardium post-myocardial infarction by inhibiting calcineurin and activating ARC.

This study investigated if acylated ghrelin (AG) could inhibit myocardial infarction (MI)-induced apoptosis in the left ventricles (LV) of male rats and tested if this protection involves modulating ARC anti-apoptotic protein. Rats (n = 12/group) were assigned as a sham-operated, a sham + AG (100 µg/kg, 2x/d, S.C.), MI, and MI + AG. With no antioxidant activity or expression of FAS, AG inhibited caspase-3, 8, and 9 and decreased cytosolic/mitochondrial levels of cytochrome-c, Bax, Bad, and Bad-BCL-2 complex in the LVs of the sham-operated and MI-treated rats. Concomitantly, AG preserved the mitochondria structure, decreased mtPTP, and enhanced state-3 respiration in the LVs of both treated groups. These effects were associated with increased mitochondrial levels of ARC and a reduction in the activity of calcineurin. Overall, AG suppresses MI-induced ventricular apoptosis by inhibition of calcineurin, activation of ARC, and preserving mitochondria integrity.

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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.