Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Department of Internal Medicine, Tianjin Port Hospital, Tianjin, China.
Hum Exp Toxicol. 2021 Sep;40(9):1485-1495. doi: 10.1177/0960327121997977. Epub 2021 Mar 17.
Myocardial ischemia is the main reason for ischemic heart diseases. Antioxidant treatment is considered as a possible approach to prevent myocardial ischemia injury, because oxidative stress is a key factor triggering it. This study was to investigate the protective effects of 3,5-dimethoxy-4-hydroxy myricanol (DHM) against oxidative stress-induced cytotoxicity on H9c2 cells and further explore its mechanisms. The oxidative stress and inflammatory response markers were detected by H2DCFDA fluorescent measurement, enzyme-linked immunosorbent assay (ELISA), real-time PCR and Western blot. Results showed DHM exerted inhibitory effects against H9c2 cell damage. Furthermore, DHM decreased oxidative stress in H9c2 cells through up-regulating protein expression of heme oxygenase-1 (HO-1) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Moreover, DHM inhibited inflammatory responses through down-regulating the protein expression of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB). DHM exerted protective activities against oxidative stress-induced cell damage, at least through decreasing oxidative stress and inhibiting inflammatory responses, indicating that DHM have the potential to be developed as therapeutic agents for the treatment of myocardial ischemia.
心肌缺血是缺血性心脏病的主要原因。抗氧化治疗被认为是预防心肌缺血损伤的一种可能方法，因为氧化应激是引发损伤的关键因素。本研究旨在探讨 3,5-二甲氧基-4-羟基杨梅醇 (DHM) 对 H9c2 细胞氧化应激诱导的细胞毒性的保护作用，并进一步探讨其机制。通过 H2DCFDA 荧光测定、酶联免疫吸附测定 (ELISA)、实时 PCR 和 Western blot 检测氧化应激和炎症反应标志物。结果表明，DHM 对 H9c2 细胞损伤具有抑制作用。此外，DHM 通过上调血红素加氧酶-1 (HO-1) 和核因子 (红系衍生 2)-样 2 (Nrf2) 的蛋白表达，降低 H9c2 细胞中的氧化应激。此外，DHM 通过下调丝裂原活化蛋白激酶 (MAPKs) 和核因子 kappa B (NF-κB) 的蛋白表达抑制炎症反应。DHM 对氧化应激诱导的细胞损伤具有保护作用，至少通过降低氧化应激和抑制炎症反应来实现，这表明 DHM 有可能被开发为治疗心肌缺血的治疗剂。
