艾利对斯坦诺佐洛尔诱导的心脏毒性的保护作用:在子模型中的生理学和病理学证据
Mohammed Hayder Asker1, Noor Al-Huda Salah Al-Zuhairy1, Wassan Mhammed Husain2
1Department of Pharmacology and Toxicology, College of Pharmacy, Mustansiriyah University Baghdad, Baghdad, Iraq.
Animal models and experimental medicine
|June 19, 2025
概括
中的一种化合物 - - 素 - - 保护子免受类固醇 stanozolol 引起的心脏损伤. 这种天然化合物减少氧化应激,炎症,并改善心脏健康标志物.
科学领域:
- 心脏病学 心脏病学
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 类固醇类固醇如 stanozolol (Winstrol) 用于肌肉建设,但会带来严重的心血管风险.
- 已知 stanozolol 诱导心脏毒性,导致心肌损伤和功能障碍.
研究的目的:
- 评估子模型中素诱导的心脏损伤对素的心脏保护作用,素是一种来自大的化合物.
- 研究氨酸的保护作用背后的机制,重点关注氧化应激,炎症和脂质代谢.
主要方法:
- 三十只子被分为对照组, stanozolol 治疗组和 stanozolol 加上 allicin 治疗组.
- 心脏功能标志物 (热波,CK,加列-3,GDF-15),氧化应激标志物 (MDA,谷氨,催化酶),炎症调解物 (CRP,IL-6,TNF-α等等). ),并评估了脂质概况.
- 组织病理学检查评估了心肌损伤,亡和纤维化.
主要成果:
- 斯坦诺佐洛尔显著增加了心脏损伤标志物,氧化应激,炎症和脂质失调 (增加了LDL/总胆固醇,降低了HDL).
- 同时服用艾利辛有效降低了氧化应激和炎症,恢复了抗氧化剂平衡,并改善了脂质概况.
- 组织病理学显示,与单独使用 stanozolol 相比,在用利治疗的子中,心肌结构得到保存,原沉积减少.
结论:
- 阿利通过抗氧化和抗炎机制显著减轻斯坦诺佐洛尔诱导的心脏毒性.
- 阿利显示出作为一种治疗剂的潜力,可以抵消与类固醇使用相关的心血管风险.
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