Sirt1/Nrf2/TNFα; TLR4/Myd88/NF-κB signaling pathways are involved in mediating hepatoprotective effect of bupropion in rat model of myocardial infarction.

IF 2.9 4区 医学 Q3 IMMUNOLOGY Immunopharmacology and Immunotoxicology Pub Date : 2024-12-01 Epub Date: 2024-10-16 DOI:10.1080/08923973.2024.2415461
Walaa Yehia Abdelzaher, Ayman Geddawy, Mina Ezzat Attya, Abdel Hamid Sayed AboBakr Ali, Doaa Mohamed Elroby Ali, Dania S Waggas, Heba K Alshaeri, Yasmine F Ibrahim
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Abstract

Background: The aim of the current study is to identify the possible protective effect of bupropion (BUP) on liver injury in rat model of myocardial infarction (MI). BUP was administered in the presence and absence of MI.

Materials and methods: Thirty-two Wistar adult male rats were randomly arranged into four groups: control, BUP (30 mg/kg/day, intraperitoneal) for 28 days, isoproterenol (ISO) was injected subcutaneous (85 mg/kg) in the 26th and 27th days and BUP/ISO groups. Cardiac and hepatic enzymes were measured, also Hepatic oxidative stress indicators, as well as inflammatory and apoptotic biomarkers, were evaluated. Cardiac and hepatic histopathological examination and hepatic nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) immunohistochemical study were also detected.

Results: ISO significantly increased cardiac and hepatic enzymes, hepatic oxidative stress, inflammatory, apoptotic, with a histopathological picture of cardiac and hepatic damage and high hepatic NF-κB immunoexpression were detected. BUP significantly normalized the upraised oxidative, inflammatory, and apoptotic parameters, with an impressive improvement in the histopathological picture and a reduction in hepatic NF-κB immunoexpression.

Conclusion: BUP protects against liver injury on top of MI in rat model via modulation of Sirtuin type 1 (Sirt1)/Nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/tumor necrosis factor α (TNFα); Toll-like receptor 4 (TLR4)/Hepatic myeloid differentiation primary response 88(Myd88)/NF-κB signaling pathways.

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Sirt1/Nrf2/TNFα;TLR4/Myd88/NF-κB 信号通路参与了安非他酮对心肌梗死大鼠模型的保肝作用。
研究背景本研究旨在确定安非他明(BUP)对心肌梗死(MI)大鼠模型肝损伤的可能保护作用。材料和方法:32 只 Wistar 成年大鼠:将 32 只 Wistar 成年雄性大鼠随机分为四组:对照组、安非他明(30 毫克/千克/天,腹腔注射)28 天组、第 26 和 27 天皮下注射异丙肾上腺素(85 毫克/千克)组以及安非他明/异丙肾上腺素组。对心脏和肝脏酶进行了测定,还评估了肝脏氧化应激指标以及炎症和细胞凋亡生物标志物。还检测了心脏和肝脏组织病理学检查以及肝脏核因子卡巴轻链-活化 B 细胞增强因子(NF-κB)免疫组化研究:结果:ISO 使心脏和肝脏酶、肝脏氧化应激、炎症、细胞凋亡明显升高,组织病理学显示心脏和肝脏受损,肝脏 NF-κB 免疫高表达。BUP 显着使升高的氧化、炎症和细胞凋亡参数恢复正常,组织病理学症状得到明显改善,肝脏 NF-κB 免疫表达降低:结论:BUP 通过调节 Sirtuin 1 型(Sirt1)/核因子(红细胞衍生 2)样 2(Nrf2)/肿瘤坏死因子 α(TNFα);Toll 样受体 4(TLR4)/肝髓样分化初级反应 88(Myd88)/NF-κB 信号通路,保护大鼠心肌梗死模型肝损伤。
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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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