Glycitein Mitigates Doxorubicin-Induced Cardiotoxicity by Mitigating Apoptosis and Inflammatory Responses in Albino Rats

IF 2.8 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Zhou Jingya, Li Peng
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Abstract

Advancements in immune and targeted therapies have significantly enhanced cancer-specific outcomes for numerous patients. However, a proportion of these therapies is associated with cardiovascular toxicities, which pose challenges in patient management. Doxorubicin, an antineoplastic agent commonly prescribed for treating malignancies, is particularly notable for its efficacy, however, clinical usage is restricted due to its myocardial toxicity. Bioactive compounds possess immense pharmacological properties and supplementation of bioactive compounds had proven to ameliorate drug-induced toxicities. In this study, we aimed to evaluate the ameliorative effect of bioactive compound glycitein against DOX-triggered myocardial toxicity. DOX-treated Wistar rats were subsequently administered with two different doses of glycitein. The change in body weight and arterial pressure was recorded. After 24 h, the last treatment animals were euthanized, blood and cardiac tissue samples were collected. The levels of C-RP, uric acid, total protein, lipid peroxidation, and antioxidants were quantified in the experimental animals to assess the impact of glycitein against DOX-induced oxidative stress. Lipid-lowering effect and ATPase-regulating effect of glycitein in DOX-administered rats were measured. Inflammatory inducers and apoptotic proteins in the DOX-administered animals were quantified to examine the anti-inflammatory and antiapoptotic effect of glycitein. Cardiac histopathological examination was performed to ratify the cardioprotective potency of glycitein against DOX. The results of our research prove glycitein treatment scavenged free radicals induced by DOX and rendered lipid-lowering, anti-inflammatory, antiapoptotic, and cardioprotective effects in the DOX-administered rats. Overall, our research concludes that glycitein is a potent bioactive compound which can be supplemented along with doxorubicin in cancer patients to prevent anticancer drug-induced cardiotoxicity.

Abstract Image

糖苷通过减轻白化大鼠的细胞凋亡和炎症反应减轻阿霉素诱导的心脏毒性
免疫和靶向治疗的进步显著提高了许多患者的癌症特异性结果。然而,这些疗法中有一部分与心血管毒性有关,这给患者管理带来了挑战。阿霉素是一种常用的治疗恶性肿瘤的抗肿瘤药物,其疗效尤其显著,但由于其心肌毒性,临床使用受到限制。生物活性化合物具有巨大的药理特性,补充生物活性化合物已被证明可以改善药物引起的毒性。在本研究中,我们旨在评估生物活性化合物glycitein对dox引发的心肌毒性的改善作用。dox处理的Wistar大鼠随后被给予两种不同剂量的糖苷。记录体重和动脉压的变化。24 h后,对最后一组处理动物实施安乐死,采集血液和心脏组织样本。定量测定实验动物C-RP、尿酸、总蛋白、脂质过氧化和抗氧化剂水平,以评估glycitein对dox诱导的氧化应激的影响。测定了甘糖素对dox大鼠的降脂作用和atp酶调节作用。定量测定dox给药动物体内的炎症诱导剂和凋亡蛋白,以检测糖苷的抗炎和抗凋亡作用。心脏组织病理学检查证实了糖苷对DOX的心脏保护作用。我们的研究结果证明,在DOX给药的大鼠中,glycitein处理可以清除DOX诱导的自由基,并具有降脂、抗炎、抗凋亡和心脏保护作用。综上所述,我们的研究表明,糖苷是一种有效的生物活性化合物,可以与阿霉素一起补充给癌症患者,以预防抗癌药物引起的心脏毒性。
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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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