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含3-β-D-吡喃葡萄糖基桔梗皂苷的生物转化根提取物在脂多糖刺激的肺泡巨噬细胞NR8383细胞中的抗炎活性

Anti-Inflammatory Activity of Biotransformed Root Extracts Containing 3--β-D-Glucopyranosyl Platycosides in LPS-Stimulated Alveolar Macrophages, NR8383 Cells.

作者信息

Choi Jeong Won, Choi Hyeok Jin, Na Chae Sun, Lee Hwan, Lee Byung Joo, Shin Kyung-Chul, Jeong Jin Boo

机构信息

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.

出版信息

J Microbiol Biotechnol. 2024 Dec 28;34(12):2609-2617. doi: 10.4014/jmb.2408.08005. Epub 2024 Oct 31.

DOI:10.4014/jmb.2408.08005
PMID:39476865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11729695/
Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/b1fed327fe05/jmb-34-12-2609-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/70f037ff4cd5/jmb-34-12-2609-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/9cf9746206de/jmb-34-12-2609-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/20019fa0861a/jmb-34-12-2609-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/4278e375d540/jmb-34-12-2609-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/a0076b1d24ea/jmb-34-12-2609-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/b1fed327fe05/jmb-34-12-2609-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/70f037ff4cd5/jmb-34-12-2609-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/9cf9746206de/jmb-34-12-2609-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/20019fa0861a/jmb-34-12-2609-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/4278e375d540/jmb-34-12-2609-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/a0076b1d24ea/jmb-34-12-2609-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4f9/11729695/b1fed327fe05/jmb-34-12-2609-f6.jpg

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