Kirenol 可缓解炎症和氧化应激,从而改善大鼠心肌缺血再灌注损伤。

IF 2.6 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Jinlong Shi, Bingfeng Guan, Minghui Gong, Xinyi He
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引用次数: 0

摘要

缺血性心脏病严重威胁人类健康,甚至导致死亡。基瑞诺主要来源于豨莶草,具有广泛的生物效应(如抗菌、抗炎、抗癌和保护心脏)。然而,基仁醇在心肌缺血再灌注损伤(MI/RI)中的调节作用和相关机制仍不清楚。本研究首先建立了心肌缺血再灌注损伤大鼠模型。结果表明,基仑诺对 MI/RI 大鼠心功能的恶化有保护作用。此外,缺血再灌注(IR)会诱发炎症,而基萘酚(5 或 10 mg/kg)同样会影响炎症。此外,缺血再灌注增强了氧化应激,而基萘酚则抵消了这一过程。接着,研究发现红外线照射后细胞凋亡增加,但这种影响被基伦诺中和。最后,研究还发现,灭蚁灵能够阻止 NF-κB 通路的激活。总之,研究揭示了基瑞诺通过调节 NF-κB 通路缓解炎症和氧化应激,从而改善大鼠的 MI/RI 状况。这项研究为寻找治疗 MI/RI 的有效药物提供了新的思路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Kirenol Alleviates Inflammation and Oxidative Stress to Improve Myocardial Ischemia/Reperfusion Injury in Rats.

Abstract: Ischemic heart disease gravely threatens human health and even results in death. Kirenol is predominantly derived from the Herba Siegesbeckiae plant species and possesses a wide range of biological effects (such as antibacterial, anti-inflammatory, anticancer, and cardioprotective). However, the regulatory effects and associated mechanisms of kirenol in myocardial ischemia/reperfusion injury (MI/RI) remain unclear. In this study, first, the MI/RI rat model was established. It was demonstrated that kirenol protected against the aggravation of cardiac function in MI/RI rats. In addition, the inflammation was induced by ischemia reperfusion (IR), which was likewise affected by kirenol (5 or 10 mg/kg). Moreover, IR enhanced oxidative stress, a process that was counteracted by kirenol. Next, cell apoptosis was discovered to be heightened after IR, but this effect was neutralized by kirenol. Finally, it was revealed that kirenol has the ability to block the activation of the NF-κB pathway. In conclusion, it was disclosed that kirenol alleviated inflammation and oxidative stress through modulating the NF-κB pathway to improve MI/RI in rats. This work may offer novel insights for searching useful drugs for treating MI/RI.

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来源期刊
CiteScore
5.10
自引率
3.30%
发文量
367
审稿时长
1 months
期刊介绍: Journal of Cardiovascular Pharmacology is a peer reviewed, multidisciplinary journal that publishes original articles and pertinent review articles on basic and clinical aspects of cardiovascular pharmacology. The Journal encourages submission in all aspects of cardiovascular pharmacology/medicine including, but not limited to: stroke, kidney disease, lipid disorders, diabetes, systemic and pulmonary hypertension, cancer angiogenesis, neural and hormonal control of the circulation, sepsis, neurodegenerative diseases with a vascular component, cardiac and vascular remodeling, heart failure, angina, anticoagulants/antiplatelet agents, drugs/agents that affect vascular smooth muscle, and arrhythmias. Appropriate subjects include new drug development and evaluation, physiological and pharmacological bases of drug action, metabolism, drug interactions and side effects, application of drugs to gain novel insights into physiology or pathological conditions, clinical results with new and established agents, and novel methods. The focus is on pharmacology in its broadest applications, incorporating not only traditional approaches, but new approaches to the development of pharmacological agents and the prevention and treatment of cardiovascular diseases. Please note that JCVP does not publish work based on biological extracts of mixed and uncertain chemical composition or unknown concentration.
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