Department of Biology, College of Science, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia.
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt.
Drug Des Devel Ther. 2024 Jul 30;18:3383-3397. doi: 10.2147/DDDT.S464334. eCollection 2024.
This comprehensive study investigated the therapeutic potential of α-asarone in mitigating myocardial oxidative damage, primarily induced by hexavalent chromium (Cr(VI)) exposure in mice.
In this experiment, 24 mice were divided into four groups to assess the cardioprotective role of α-asarone. The study focused on two treatment groups, receiving 25 mg and 50 mg of α-asarone, respectively. These groups were compared against a control group subjected to Cr(VI) without α-asarone treatment, and a normal control negative group. The key biochemical parameters evaluated included serum levels of Creatine Kinase-MB (CK-MB) and Troponin I, markers indicative of myocardial damage. Additionally, the levels of Malondialdehyde (MDA) were measured to assess lipid peroxidation, alongside the evaluation of key inflammatory biomarkers in cardiac tissue homogenates, such as Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β). Remarkably, α-asarone treatment resulted in a significant reduction in these markers compared to the control group. The treatment also elevated the activity of cardinal antioxidant enzymes like catalase (CAT) and superoxide dismutase (SOD), and reduced the glutathione (GSH). Furthermore, a notable upregulation of Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) in cardiac tissue homogenates was observed, highlighting a potential pathway through which α-asarone exerts its protective effects. Histopathological analysis of cardiac tissues revealed that α-asarone ameliorated the structural lesions induced by Cr(VI). The study thus provides substantial evidence that α-asarone ameliorates Cr(VI)-induced cardiotoxicity through a multifaceted approach. It enhances cardiac enzyme function, modulates free radical generation, improves antioxidant status, and mitigates histopathological damage in cardiac tissues. Given these findings, α-asarone emerges as a promising agent against Cr(VI)-induced myocardial injury.
This study paves the way for further research into the cardioprotective properties of α-asarone and its potential application in clinical settings by specifically exploring the protective efficacy of α-asarone against Cr(VI)-induced cardiotoxicity and delineating the underlying biochemical and molecular mechanisms involved.
本综合研究旨在探讨α-细辛脑在减轻小鼠六价铬(Cr(VI))暴露引起的心肌氧化损伤方面的治疗潜力。
本实验将 24 只小鼠分为四组,以评估α-细辛脑的心脏保护作用。研究重点关注两个治疗组,分别给予 25mg 和 50mg 的α-细辛脑,同时设立 Cr(VI)处理但未给予α-细辛脑的对照组,以及正常对照阴性组。评估的关键生化参数包括血清肌酸激酶同工酶(CK-MB)和肌钙蛋白 I 水平,这是心肌损伤的标志物。此外,还测定了丙二醛(MDA)水平以评估脂质过氧化,同时评估心脏组织匀浆中的关键炎症生物标志物,如肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)。值得注意的是,与对照组相比,α-细辛脑治疗显著降低了这些标志物的水平。治疗还提高了关键抗氧化酶如过氧化氢酶(CAT)和超氧化物歧化酶(SOD)的活性,并降低了谷胱甘肽(GSH)的水平。此外,还观察到心脏组织匀浆中过氧化物酶体增殖物激活受体γ(PPAR-γ)的显著上调,这突出了α-细辛脑发挥其保护作用的潜在途径。心脏组织的组织病理学分析表明,α-细辛脑改善了 Cr(VI)引起的结构损伤。因此,该研究提供了充分的证据表明,α-细辛脑通过多方面的途径减轻 Cr(VI)引起的心脏毒性。它增强了心肌酶的功能,调节自由基的产生,改善了抗氧化状态,并减轻了心脏组织的组织病理学损伤。鉴于这些发现,α-细辛脑作为一种有前途的抗 Cr(VI)诱导心肌损伤的药物脱颖而出。
本研究通过具体探讨α-细辛脑对 Cr(VI)诱导的心脏毒性的保护作用,并阐明其中涉及的生化和分子机制,为进一步研究α-细辛脑的心脏保护特性及其在临床环境中的潜在应用奠定了基础。