Amelioration of Isoproterenol-Induced Myocardial Infarction by the Phytochemical Koenigicine via Modulation of NF-κB/HO-1/NQO-1 Pathways: An In Vivo Analysis

IF 3.2 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Tianming Hu, Lan Liu
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Abstract

Phytochemicals exhibit diverse cardioprotective properties that contribute to the prevention and management of myocardial infarction (MI). In our study, we examined the potency of the phytochemical Koenigicine, which belongs to the carbazole alkaloid, in alleviating MI in an animal model. The animals were supplemented with Koenigicine before MI induction using isoproterenol, with supplementation continuing during the MI induction period. The impact of Koenigicine on mitigating the onset of MI was evaluated by quantifying lipid levels and arterial blood pressure. Its ameliorative potential against isoproterenol-induced cardiac damage was assessed by measuring antioxidant levels and critical biomarkers of MI in the experimental animals. Protein, C-reactive protein (CRP), and uric acid levels were assessed to determine the effect of Koenigicine on immune function and inflammation. Additionally, the impact of Koenigicine on cardiac muscle function and its role in healing ischemic-induced cardiac tissues were examined in MI-induced rats. The effect of Koenigicine treatment on post-ischemic injury was analyzed by quantifying NF-κB, HO-1, and NQO-1 levels, and the findings were confirmed through cardiac histopathological analysis. Koenigicine administration effectively mitigated MI induction by regulating lipid levels and arterial blood pressure. It enhanced the antioxidant defense system, attenuated inflammatory signaling, and thereby prevented MI-induced cardiac tissue damage. The results of MI biomarker analysis confirmed the ameliorative potential of Koenigicine against isoproterenol-induced cardiac inflammation. Furthermore, it demonstrated a positive effect on cardiac function and facilitated the healing process following MI induction. Overall, our findings suggest that Koenigicine provides preventive, suppressive, and ameliorative effects at all stages of MI, addressing gaps in the efficacy of currently available treatments.

Abstract Image

异丙肾上腺素通过调节NF-κB/HO-1/NQO-1通路改善异丙肾上腺素诱导心肌梗死的体内研究
植物化学物质表现出多种心脏保护特性,有助于预防和管理心肌梗死(MI)。在我们的研究中,我们在动物模型中检测了植物化学物Koenigicine(属于咔唑生物碱)缓解心肌梗死的效力。动物在异丙肾上腺素诱导心肌梗死前补充柯尼辛,并在心肌梗死诱导期间继续补充。通过量化脂质水平和动脉血压来评估柯尼辛对缓解心肌梗死发作的影响。通过测量实验动物的抗氧化水平和心肌梗死的关键生物标志物,评估其对异丙肾上腺素诱导的心脏损伤的改善潜力。评估蛋白、c反应蛋白(CRP)和尿酸水平,以确定柯尼西嗪对免疫功能和炎症的影响。此外,我们还观察了柯尼希碱对心肌缺血大鼠心肌功能的影响及其在心肌组织修复中的作用。通过量化NF-κB、HO-1、NQO-1水平分析柯尼西嗪治疗对缺血后损伤的影响,并通过心脏组织病理学分析证实上述结果。柯尼辛通过调节血脂水平和动脉血压有效减轻心肌梗死的诱导。它增强抗氧化防御系统,减弱炎症信号,从而防止心肌梗死引起的心脏组织损伤。MI生物标志物分析的结果证实了柯尼辛对异丙肾上腺素诱导的心脏炎症的改善潜力。此外,它对心功能有积极作用,并促进心肌梗死诱导后的愈合过程。总的来说,我们的研究结果表明,柯尼辛在心肌梗死的所有阶段都具有预防、抑制和改善作用,解决了目前可用治疗方法疗效上的差距。
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来源期刊
CiteScore
5.80
自引率
2.80%
发文量
277
审稿时长
6-12 weeks
期刊介绍: The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.
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