Lim Jae Sung, Lee Sung Ho, Yun Hyosuk, Lee Da Young, Cho Namki, Yoo Guijae, Choi Jeong Uk, Lee Kwang Youl, Bach Tran The, Park Su-Jin, Cho Young-Chang
College of Pharmacy and Research Institute of Pharmaceutical Sciences, Chonnam National University, 77 Yongbong-ro, Gwangju 61186, Republic of Korea.
Department of Chemistry, Chonnam National University, Gwangju 61186, Republic of Korea.
Antioxidants (Basel). 2023 Sep 22;12(10):1792. doi: 10.3390/antiox12101792.
() L., an evergreen tree with substantial biological activity, including antioxidant and anti-inflammatory effects, has been used in many herbal and traditional medicines. To elucidate its antioxidant and anti-inflammatory activity and the underlying mechanisms, we applied a methanol extract of (ETME) to lipopolysaccharide (LPS)-stimulated mouse immortalized Kupffer cells. ETME suppressed the LPS-induced increase in nitric oxide, a mediator for oxidative stress and inflammation, and restored LPS-mediated depletion of total glutathione level by stabilizing antioxidative nuclear factor erythroid 2-related factor 2 (Nrf2) and the subsequent increase in heme oxygenase-1 levels. Furthermore, ETME inhibited the LPS-induced production of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1β, and IL-6. The inhibitory effects of ETME on pro-inflammatory responses were regulated by ETME-mediated dephosphorylation of mitogen-activated protein kinases (MAPKs: p38, p44/p42, and stress-associated protein kinase/c-Jun N-terminal kinase) and inhibition of nuclear localization of nuclear factor kappa B (NF-κB). These results suggest that ETME is a possible candidate for protecting Kupffer cells from LPS-mediated oxidative stress and excessive inflammatory responses by activating antioxidant Nrf2/HO-1 and inhibiting pro-inflammatory NF-κB and MAPKs, respectively.
（）L.是一种具有多种生物活性的常绿树，包括抗氧化和抗炎作用，已被用于许多草药和传统药物中。为了阐明其抗氧化和抗炎活性及其潜在机制，我们将（）的甲醇提取物（ETME）应用于脂多糖（LPS）刺激的小鼠永生化库普弗细胞。ETME抑制了LPS诱导的一氧化氮增加，一氧化氮是氧化应激和炎症的介质，并通过稳定抗氧化核因子红细胞2相关因子2（Nrf2）以及随后血红素加氧酶-1水平的增加，恢复了LPS介导的总谷胱甘肽水平的消耗。此外，ETME抑制了LPS诱导的促炎细胞因子的产生，包括肿瘤坏死因子-α、白细胞介素（IL）-1β和IL-6。ETME对促炎反应的抑制作用是通过ETME介导的丝裂原活化蛋白激酶（MAPKs：p38、p44/p42和应激相关蛋白激酶/c-Jun N端激酶）的去磷酸化以及对核因子κB（NF-κB）核定位的抑制来调节的。这些结果表明，ETME可能是一种候选物，通过分别激活抗氧化剂Nrf2/HO-1和抑制促炎NF-κB和MAPKs，保护库普弗细胞免受LPS介导的氧化应激和过度炎症反应。
