Qian Kai, Song Li, Guo Jia-Min, Fu Dan, Shi Jia, Ma Yu, Ge Zi-Jie, Li Lei, Zhang Su-Qin
Department of Cardiology, Key Laboratory of Panvascular Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China.
Medical College of YiChun University, YiChun, Jiang Xi, 336000, China.
BMC Cardiovasc Disord. 2024 Dec 20;24(1):733. doi: 10.1186/s12872-024-04395-9.
Cardiovascular disease carries the highest mortality rate among diseases, and pharmacological interventions have limited efficacy. Baicalin (Bai) promotes biological metabolic processes, eliminates oxygen free radicals, and is anti-inflammatory. This study aimed to investigate the effect of Bai on the cardiac injury model induced by isoproterenol in mice.
In this study, all groups except the control received intraperitoneal injections of isoproterenol (ISO) to induce a cardiac injury model, with the drug administered continuously for 14 days. hematoxylin and eosin staining and Masson's trichrome staining revealed that Bai significantly mitigated ISO-induced pathological changes in mouse heart tissue and alleviated myocardial hypertrophy. Echocardiography assessments demonstrated that Bai preserved cardiac function in ISO-treated mice. Furthermore, our findings indicated that Bai activated the Nrf2 signaling pathway in vivo and in vitro. To delve deeper, mice were further treated with ML385 (ML) via intraperitoneal injection to inhibit the Nrf2 pathway. Results showed that ML385 blocked the cardioprotective effects of Bai in mouse heart tissue.
Bai protects against ISO-induced cardiac injury, and its mechanism is related to activating the Nrf2/HO-1 signaling pathway to regulate cardiac ferroptosis and improve cardiac remodeling.
心血管疾病是死亡率最高的疾病，药物干预疗效有限。黄芩苷可促进生物代谢过程，清除氧自由基，并具有抗炎作用。本研究旨在探讨黄芩苷对异丙肾上腺素诱导的小鼠心脏损伤模型的影响。
在本研究中，除对照组外，所有组均腹腔注射异丙肾上腺素（ISO）以诱导心脏损伤模型，并连续给药14天。苏木精-伊红染色和Masson三色染色显示，黄芩苷显著减轻了ISO诱导的小鼠心脏组织病理变化，并减轻了心肌肥大。超声心动图评估表明，黄芩苷可维持ISO处理小鼠的心脏功能。此外，我们的研究结果表明，黄芩苷在体内和体外均激活了Nrf2信号通路。为了进一步深入研究，通过腹腔注射对小鼠进一步给予ML385（ML）以抑制Nrf2通路。结果显示，ML385阻断了黄芩苷对小鼠心脏组织的心脏保护作用。
黄芩苷可预防ISO诱导的心脏损伤，其机制与激活Nrf2/HO-1信号通路以调节心脏铁死亡和改善心脏重塑有关。
