Abstract
The phytochemical investigation on the methanol extract of the rhizomes of Atractylodes macrocephala resulted in the discovery of one new compound 9α-hydroxyatractylenolide (1) and 21 known compounds including atractylone (2), 3β-acetoxyatractylon (3), atractylenolide I (4), atractylenolide II (5), 8-epiasterolid (6), atractylenolide III (7), atractylenolide VII (8), 8-epiatractylenolide III (9), eudesm-4(15)-ene-7α,11-diol (10), linoleic acid (11), myristic acid (12), 3-O-caffeoyl-1-methyquinic acid (13), (2E,8E,10E)-tetradecatriene-4,6-diyne-1,14-diol (14), 14-aceroxy-12-senecioyloxytetradeca-2E,8Z,10E-trien-4,6-diyn-1-ol (15), isoscopoletin (16), caffeic acid (17), protocatechic acid (18), 3-O-caffeoylquinic acid (19), 4-O-caffeoylquinic acid (20), 1,5-di-O-caffeoylquinic acid (21), and nicotinic acid (22). Their structures were identified using nuclear magnetic resonance (NMR) and mass spectroscopy, and by comparison with previously published data. Compounds 4, 5, 6, 8, and 10–22 significantly inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW264.7 macrophages, and compounds 4, 5, 6, 16, and 17 showed those responses in BV2 microglial cells. Especially, compound 6 showed the second-best effect, and inhibited the LPS-induced production of prostaglandin E2 (PGE2), the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and the production of cytokines including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in both cells. These inhibitory effects were mediated by the inactivation of nuclear factor kappa B (NF-κB) signaling pathway.
Highlights
IntroductionInflammation is associated with the activation of macrophages or monocytes that are responsible for the innate and adaptive immune responses of the human body
Inflammation is associated with the activation of macrophages or monocytes that are responsible for the innate and adaptive immune responses of the human body.Following various stimuli, these immune cells release a series of pro-inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, chemokines, and signaling-associated proteins [1] to protect the infected tissues site and to maintain the homeostasis of the body [2]
The pre-treatment with 8-epiasterolid did not inhibit the activation of all three mitogen-activated protein kinase (MAPK) (Fig. 8). In this investigation, we isolated 22 compounds from the rhizomes of A. macrocephala using various combined chromatographic methods, and evaluated their anti-inflammatory effects measuring the degree of the production of NO in LPS-induced RAW264.7 and
Summary
Inflammation is associated with the activation of macrophages or monocytes that are responsible for the innate and adaptive immune responses of the human body. Following various stimuli, these immune cells release a series of pro-inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, chemokines, and signaling-associated proteins [1] to protect the infected tissues site and to maintain the homeostasis of the body [2]. Macrophages and microglia are important sources of pro-inflammatory mediators through the activation of transcription factors such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) due to lipopolysaccharide (LPS) stimulation [7, 8]. Since macrophages and microglia stimulated by LPS produce excessive pro-inflammatory mediators, they are being utilized in in vitro models to evaluate the effectiveness of potentially anti-inflammatory candidate substances [10, 11]
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