Choi Jeong Won, Choi Hyeok Jin, Na Chae Sun, Lee Hwan, Lee Byung Joo, Shin Kyung-Chul, Jeong Jin Boo
Department of Forest Science, Andong National University, Andong 36729, Republic of Korea.
Division of Wild Plant and Seeds, Baekdudaegan National Arboretum, Bonghwa 36029, Republic of Korea.
J Microbiol Biotechnol. 2024 Dec 28;34(12):2609-2617. doi: 10.4014/jmb.2408.08005. Epub 2024 Oct 31.
Acute lung injury (ALI) is a severe inflammatory condition characterized by excessive immune responses and oxidative stress, leading to significant tissue damage. Given the need for novel therapeutic agents, this study aimed to explore the anti-inflammatory activity and mechanisms of biotransformed root extracts (BT-PGR), which were enzymatically processed using rapidsase PL Classic from . The goal was to assess the potential of BT-PGR as a natural treatment for ALI. BT-PGR effectively inhibited the production of NO, iNOS, IL-1β, IL-6, and TNF-α induced by LPS in NR8383 cells. BT-PGR inhibited the phosphorylation of ERK1/2, p38, JNK and p65 in LPS-stimulated NR8383 cells. In addition, BT-PGR suppressed LPS-mediated activation of NF-κB luciferase activity. BT-PGR increased the levels of HO-1 and the inhibition of HO-1 by ZnPP attenuated BT-PGR-mediated inhibition of NO production. In addition, the inhibition of PI3K by LY294002 blocked the BT-PGR-mediated increase of HO-1 level. BT-PGR increased nuclear Nrf2 level and the knockdown of Nrf2 by siRNA inhibited BT-PGR-mediated increase of HO-1 level. In addition, inhibition of PI3K by LY294002 suppressed the increase of nuclear Nrf2 level. Based on these results, it can be inferred that BT-PGR exhibits anti-inflammatory activity in rat alveolar macrophages, suggesting its potential as a natural candidate for the improvement of ALI.
急性肺损伤(ALI)是一种严重的炎症状态,其特征为过度的免疫反应和氧化应激,会导致显著的组织损伤。鉴于对新型治疗药物的需求,本研究旨在探索经生物转化的根提取物(BT-PGR)的抗炎活性及其机制,该提取物是使用来自[具体来源未提及]的Rapidsase PL Classic酶法处理得到的。目的是评估BT-PGR作为ALI天然治疗方法的潜力。BT-PGR有效抑制了脂多糖(LPS)诱导的NR8383细胞中一氧化氮(NO)、诱导型一氧化氮合酶(iNOS)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的产生。BT-PGR抑制了LPS刺激的NR8383细胞中细胞外信号调节激酶1/2(ERK1/2)、p38、c-Jun氨基末端激酶(JNK)和p65的磷酸化。此外,BT-PGR抑制了LPS介导的核因子κB(NF-κB)荧光素酶活性的激活。BT-PGR增加了血红素加氧酶-1(HO-1)的水平,而锌原卟啉(ZnPP)对HO-1的抑制减弱了BT-PGR介导的对NO产生的抑制。此外,LY294002对磷脂酰肌醇3-激酶(PI3K)的抑制阻断了BT-PGR介导的HO-1水平的升高。BT-PGR增加了细胞核中核因子E2相关因子2(Nrf2)的水平,而小干扰RNA(siRNA)对Nrf2的敲低抑制了BT-PGR介导的HO-1水平的升高。此外,LY294002对PI3K的抑制抑制了细胞核中Nrf2水平的升高。基于这些结果,可以推断BT-PGR在大鼠肺泡巨噬细胞中表现出抗炎活性,表明其作为改善ALI的天然候选物的潜力。