Cardiovascular‐related diseases continue to be a leading cause of death globally. Among ischemic‐induced cardiac diseases, myocardial infarction (MI) is reported to be of an alarming value. Despite numerous improvements in the medical intrusions, still this armamentarium fails to be effective in managing the illness without setbacks. Ferruginol (FGL) is a major polyphenols and terpenoids with numerous pharmacological activities including antioxidant and anti‐inflammatory. Following, this work was aimed to explore the cardio protective effect of FGL (50 mg/kg) in isoprenaline hydrochloride (ISO)‐induced MI in experimental rats. After treatment with FGL in ISO‐induced MI in rats, noticeable changes were observed in the experimental rats. Injection of ISO to rats resulted in the augmented cardiac weight, serum cardiac markers (creatine kinase, creatine kinase‐MB, cardiac troponin T, and Cardiac troponin I), lipid peroxidation end products (thiobarbituric acid‐reactive substance and lipid hydroperoxides), reduced endogenous antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione), reduced ATPase activity, and escalated pro‐inflammatory cytokines (interleukin‐6, tumor necrosis factor‐α, and nuclear factor‐κB) levels. Interestingly, the FGL supplementation to the ISO‐treated rats revealed the diminished heart weight, reduced cardiac markers, and lipid peroxidation. FGL also possessed the improved antioxidants status and diminished pro‐inflammatory mediator levels. The outcomes of histological analysis also evidenced the cardio protective role of FGL. Treatment with FGL reduced the cardiac damage biomarkers maintained to near normal levels in ISO‐induced rats. These study findings disclose the prospective capability of FGL in the treatment of MI in the future.

中文翻译：

---

铁杉醇对盐酸异丙肾上腺素致大鼠心肌梗死的改善作用

心血管相关疾病仍然是全球主要的死亡原因。在缺血性诱发的心脏病中，据报道心肌梗塞 (MI) 具有惊人的价值。尽管在医疗入侵方面取得了许多改进，但这种医疗设备仍然无法有效地控制疾病而不会遇到挫折。Ferruginol (FGL) 是一种主要的多酚和萜类化合物，具有多种药理活性，包括抗氧化和抗炎。接下来，这项工作旨在探索 FGL（50 mg/kg）对盐酸异丙肾上腺素（ISO）诱导的实验大鼠心肌梗死的心脏保护作用。在 ISO 诱导的大鼠 MI 中用 FGL 治疗后，在实验大鼠中观察到明显的变化。向大鼠注射 ISO 导致心脏重量、血清心脏标志物（肌酸激酶、肌酸激酶-MB、心肌肌钙蛋白 T 和心肌肌钙蛋白 I）、脂质过氧化终产物（硫代巴比妥酸反应性物质和脂质氢过氧化物）、减少的内源性抗氧化剂（超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽）、降低的 ATP 酶活性，和升高的促炎细胞因子（白介素-6、肿瘤坏死因子-α和核因子-κB）水平。有趣的是，向 ISO 治疗的大鼠补充 FGL 显示心脏重量减轻、心脏标志物减少和脂质过氧化。FGL 还具有改善的抗氧化剂状态和减少的促炎介质水平。组织学分析的结果也证明了 FGL 的心脏保护作用。在 ISO 诱导的大鼠中，FGL 治疗降低了维持在接近正常水平的心脏损伤生物标志物。