Cardioprotective effect of tofisopam against isoprenaline-induced myocardial infarction in rats via modulation of NLRP3\IL-1β\caspase-1 pathway.

IF 2.9 4区 医学 Q3 IMMUNOLOGY Immunopharmacology and Immunotoxicology Pub Date : 2024-12-01 Epub Date: 2024-11-05 DOI:10.1080/08923973.2024.2421528
Alyaa Abdelfattah Abdelmonaem, Asmaa Mohamed Abdel-Aziz, Yasmine F Ibrahim, Walaa Yehia Abdelzaher, Nada Amgad Mohammed, Heba Marey, Asmaa S Taghian, Amr Setouhi, Ashraf Radi, Sara M Ahmed
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Abstract

Purpose: Cardiovascular diseases (CVDs) are a leading cause of morbidity and mortality worldwide. Ischemic heart diseases, particularly acute myocardial infarction (MI), represent the most common cause of death. MI is influenced by multiple factors, including the release of inflammatory mediators. A significant percentage of individuals with CVD experience psychological effects, such as anxiety and depression, which are linked to an increased risk of coronary heart disease. Certain anti-anxiety medications have demonstrated immunomodulatory and anti-inflammatory effects. Tofisopam, a 2,3-benzodiazepine with anxiolytic properties, has been shown to exert in vitro anti-inflammatory and immunomodulatory effects. The present study investigates the potential of tofisopam as a protective adjuvant against isoprenaline-induced MI in rats and explores the possible underlying mechanisms.

Methods: The study included four groups: a control group, a group pretreated with tofisopam, an isoprenaline toxic group, and an isoprenaline toxic group pretreated with tofisopam.

Results: The findings demonstrated that isoprenaline significantly increased cardiac enzyme levels, as well as elevated oxidative and inflammatory stress parameters, along with evident apoptosis in cardiac cells. In contrast, the tofisopam-pretreated group showed a significant reversal of the cardiac damage induced by isoprenaline.

Conclusions: Tofisopam protects against isoprenaline-induced MI through its antioxidant, anti-inflammatory, and anti-apoptotic properties.

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托非索泮通过调节 NLRP3\IL-1β\caspase-1 通路对异丙肾上腺素诱发的大鼠心肌梗死有保护作用
目的 心血管疾病(CVDs)是全球发病率和死亡率的主要原因。缺血性心脏病,尤其是急性心肌梗死(MI),是最常见的死亡原因。心肌梗死受多种因素影响,包括炎症介质的释放。有相当一部分心血管疾病患者会受到焦虑和抑郁等心理影响,这与冠心病风险的增加有关。某些抗焦虑药物具有免疫调节和抗炎作用。托非索泮是一种具有抗焦虑特性的 2,3-苯并二氮杂卓,已被证明具有体外抗炎和免疫调节作用。本研究调查了托菲索泮作为异丙肾上腺素诱导的大鼠心肌梗死保护性佐剂的潜力,并探讨了可能的内在机制。研究方法研究包括四组:对照组、托非索泮预处理组、异丙肾上腺素毒性组和托非索泮预处理的异丙肾上腺素毒性组。结果显示研究结果表明,异丙肾上腺素会明显增加心肌酶水平,并升高氧化应激和炎症应激参数,同时心肌细胞明显凋亡。相比之下,托非索泮预处理组则明显逆转了异丙肾上腺素诱发的心脏损伤。结论托非索泮具有抗氧化、抗炎和抗细胞凋亡的特性,可防止异丙肾上腺素诱发的心肌梗死。
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来源期刊
CiteScore
5.40
自引率
0.00%
发文量
133
审稿时长
4-8 weeks
期刊介绍: The journal Immunopharmacology and Immunotoxicology is devoted to pre-clinical and clinical drug discovery and development targeting the immune system. Research related to the immunoregulatory effects of various compounds, including small-molecule drugs and biologics, on immunocompetent cells and immune responses, as well as the immunotoxicity exerted by xenobiotics and drugs. Only research that describe the mechanisms of specific compounds (not extracts) is of interest to the journal. The journal will prioritise preclinical and clinical studies on immunotherapy of disorders such as chronic inflammation, allergy, autoimmunity, cancer etc. The effects of small-drugs, vaccines and biologics against central immunological targets as well as cell-based therapy, including dendritic cell therapy, T cell adoptive transfer and stem cell therapy, are topics of particular interest. Publications pointing towards potential new drug targets within the immune system or novel technology for immunopharmacological drug development are also welcome. With an immunoscience focus on drug development, immunotherapy and toxicology, the journal will cover areas such as infection, allergy, inflammation, tumor immunology, degenerative disorders, immunodeficiencies, neurology, atherosclerosis and more. Immunopharmacology and Immunotoxicology will accept original manuscripts, brief communications, commentaries, mini-reviews, reviews, clinical trials and clinical cases, on the condition that the results reported are based on original, clinical, or basic research that has not been published elsewhere in any journal in any language (except in abstract form relating to paper communicated to scientific meetings and symposiums).
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