Zhang Xinwei, He Junjie, Xu Zhen, Yang Yanna
Department of Cardiology, Lianshui People's Hospital Affiliated to Kangda College of Nanjing Medical University, No. 6 Hongri Avenue, Lianshui County, Huai'an City, 223400 Jiangsu Province China.
Cytotechnology. 2025 Jun;77(3):103. doi: 10.1007/s10616-025-00762-2. Epub 2025 May 16.
Myocardial ischemia-reperfusion injury (MI/RI) is a crucial complication of reperfusion treatment for myocardial infarction. Naringin (Nar) is a flavonoid with identified cardioprotective functions. This study aimed to explore the protective mechanisms of Nar against MI/RI, specifically focusing on its modulation of the cGAS-STING pathway. An H9c2 cardiomyocyte hypoxia/reoxygenation (H/R) injury model and an MI/R rat model were established. Our findings demonstrated that Nar, at a concentration of 480 μM, exhibited no cytotoxic effects on H9c2 cardiomyocytes and did not inhibit cell proliferation. Nar significantly reduced myocardial cell injury by improving mitochondrial function and decreasing oxidative stress, particularly the stress induced by a ferroptosis activator (Erastin). Additionally, the in vivo MI/R rat model further confirmed that Nar inhibited the activation of the cGAS-STING pathway, thereby attenuating myocardial injury. Collectively, Nar exerts protective effects against MI/RI by regulating mitochondrial dysfunction and ferroptosis, primarily through inhibition of the cGAS-STING pathway.
心肌缺血再灌注损伤（MI/RI）是心肌梗死再灌注治疗的一种关键并发症。柚皮苷（Nar）是一种具有明确心脏保护功能的类黄酮。本研究旨在探讨Nar对MI/RI的保护机制，特别关注其对cGAS-STING通路的调节作用。建立了H9c2心肌细胞缺氧/复氧（H/R）损伤模型和MI/R大鼠模型。我们的研究结果表明，浓度为480μM的Nar对H9c2心肌细胞无细胞毒性作用，且不抑制细胞增殖。Nar通过改善线粒体功能和降低氧化应激，特别是铁死亡激活剂（埃拉斯汀）诱导的应激，显著减轻心肌细胞损伤。此外，体内MI/R大鼠模型进一步证实，Nar抑制cGAS-STING通路的激活，从而减轻心肌损伤。总体而言，Nar主要通过抑制cGAS-STING通路，调节线粒体功能障碍和铁死亡，对MI/RI发挥保护作用。
