Abstract
The phytochemical investigation on the roots of Acanthopanax henryi (Araliaceae) resulted in the discovery of twenty compounds whose chemical structures were elucidated by the analysis of 1D-, 2D-NMR, mass spectrometry data, other physicochemical properties, and a comparison of the spectral data with the literature. They were identified as (-)-sesamin (1), helioxanthin (2), savinin (3), taiwanin C (4), 6-methoxy-7-hydroxycoumarin (5), behenic acid (6), 3-O-caffeoyl-quinic acid (7), 5-O-caffeoyl-quinic acid (8), 1,3-di-O-caffeoyl-quinic acid (9), 1,4-di-O-caffeoyl-quinic acid (10), 1,5-di-O-caffeoyl-quinic acid (11), (+)-threo-(7R,8R)-guaiacylglycerol-β-coniferyl aldehyde ether (12), (+)-erythro-(7S,8R)-guaiacylglycerol-β-coniferyl aldehyde ether (13), ferulic acid (14), caffeic acid (15), stigmasterol (16), β-sitosterol (17), adenosine (18), syringin (19), and trans-coniferin (20). Among these isolates, compound 3 showed inhibitory activity against lipopolysaccharide- (LPS-) induced nitric oxide (NO) and prostaglandin E2 (PGE2) production with IC50 values of 2.22 ± 0.11 and 2.28 ± 0.23 μM, respectively. The effects of compound 3 were associated with the suppression of LPS-induced expression of the inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein. Furthermore, compound 3 negatively regulated the production of interleukin- (IL-) 1β and tumor-necrosis factor- (TNF-) α at the transcriptional level in LPS-stimulated BV2 microglial cells. These antineuroinflammatory effects of compound 3 were mediated by p38 mitogen-activated protein kinase (MAPK).
Highlights
Neuroinflammatory responses are mainly mediated by microglial activation, and they are implicated in the development of neurodegenerative diseases such as Alzheimer’s diseases (AD), Parkinson’s disease (PD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS) [1]
20 secondary metabolites were isolated from the EtOAc, butanol, and PE-soluble fractions of the methanol extract of Acanthopanax henryi roots
Savinin was the only compound which inhibited the production of nitric oxide (NO) and PGE2, and the expression of inducible nitric oxide synthase (iNOS) and COX-2 proteins in LPS-stimulated BV2 microglial cells
Summary
Neuroinflammatory responses are mainly mediated by microglial activation, and they are implicated in the development of neurodegenerative diseases such as Alzheimer’s diseases (AD), Parkinson’s disease (PD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS) [1]. Activated microglia produce excess immune reactions which are detrimental to brain tissue and can produce various proinflammatory mediators such as tumor necrosis factor(TNF-) α, interleukins (ILs), nitric oxide (NO), prostaglandin. E2 (PGE2), and reactive oxygen species (ROS). Released and accumulated, these proinflammatory mediators facilitate the development of neurodegenerative diseases [3, 4]. It is important to suppress the secretion of proinflammatory mediators from activated microglial cells to prevent the neuroinflammation-related development of neurodegenerative diseases
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More From: Evidence-based complementary and alternative medicine : eCAM
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