Yu Ga-Ram, Lee Seung-Jun, Kim Da-Hoon, Lim Dong-Woo, Kim Hyuck, Park Won-Hwan, Kim Jai-Eun
Department of Diagnostics, College of Korean Medicine, Dongguk University, Dongguk-Ro 32, Goyang 10326, Republic of Korea.
Department of Pathology, College of Korean Medicine, Dongguk University, Dongguk-Ro 32, Goyang 10326, Republic of Korea.
Evid Based Complement Alternat Med. 2020 Dec 7;2020:8881683. doi: 10.1155/2020/8881683. eCollection 2020.
Relatively high proportions of proinflammatory M1-like macrophages in tissues may lead to vascular impairment and trigger numerous diseases including atherosclerosis-related cardiovascular disease (CVD). Jisil Haebaek Gyeji-tang (JHGT), a polyherbal decoction, is traditionally used to treat various human ailments including chest pain, angina, and myocardial infarction. In the present study, we investigated the anti-inflammatory effects of JHGT on lipopolysaccharide- (LPS-) stimulated M1 macrophage polarization generated via the mitogen-activated protein kinases (MAPKs) pathway in RAW 264.7 mouse macrophages. The reducing power of JHGT was also investigated using DAF-FA DA in a zebrafish model. JHGT significantly reduced inflammatory mediator levels, including iNOS, COX2, TNF-, IL-6, and IL-1, as compared with LPS-stimulated controls in vitro and ex vivo. Furthermore, JHGT suppressed the ERK1/2, JNK, and p38 MAPK pathways and reduced p-IB levels and the nuclear translocation of NF-B in RAW 264.7 cells. In addition, treatment with JHGT significantly reduced the NO levels in LPS-treated zebrafish larva ex vivo. Our findings show the potent anti-inflammatory properties of JHGT are due to its suppression of MAPK signaling, NF-B translocation, and M1 macrophage polarization.
组织中促炎M1样巨噬细胞比例相对较高可能导致血管损伤，并引发包括动脉粥样硬化相关心血管疾病（CVD）在内的多种疾病。济世还魄桂技汤（JHGT）是一种多草药煎剂，传统上用于治疗各种人类疾病，包括胸痛、心绞痛和心肌梗死。在本研究中，我们研究了JHGT对脂多糖（LPS）刺激的RAW 264.7小鼠巨噬细胞中通过丝裂原活化蛋白激酶（MAPKs）途径产生的M1巨噬细胞极化的抗炎作用。还使用DAF-FA DA在斑马鱼模型中研究了JHGT的还原能力。与体外和体内LPS刺激的对照组相比，JHGT显著降低了包括诱导型一氧化氮合酶（iNOS）、环氧化酶2（COX2）、肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和白细胞介素-1（IL-1）在内的炎症介质水平。此外，JHGT抑制了RAW 264.7细胞中的细胞外信号调节激酶1/（ERK1/2）、c-Jun氨基末端激酶（JNK）和p38丝裂原活化蛋白激酶途径，并降低了IκB磷酸化水平和核因子-κB（NF-κB）的核转位。此外，JHGT处理显著降低了体内LPS处理的斑马鱼幼虫中的一氧化氮（NO）水平。我们的研究结果表明，JHGT的强大抗炎特性归因于其对MAPK信号传导、NF-κB转位和M1巨噬细胞极化的抑制作用。
