ABSTRACT
Objective To study the chemical constituents of Gendarussa vulgaris. Methods The chemical constituents were isolated and purified with silica column chromatography and gel chromatography, etc. Their structures were identified by physico- chemical properties and various spectroscopic methods including NMR spectrum, MS, UV, etc. Results A total of 16 compounds were isolated and elucidated as daucosterol (1), 6″-O-acetylisavitexin (2), 9,10-dihydroxy-4,7-megastigmadien-3-one (3), 22E,24R-ergosta- 7,22-diene-3β,5α,6β,9α-tetraol (4), isorhamnetin (5), quercetin (6), eleutheroside E (7), gusanlung A (8), gusanlung B (9), betulin (10), isovitexin-2″-O-rhamnoside (11), isovitexin (12), genkwanin (13), apigenin (14), quercetin 3-O-β-D-glucuronide (15), and 2-(4-hydroxy-3-methoxyphenyl)-3-(2-hydroxy-5-methoxyphe-nyl)-3-oxo-1-propanol (16). Conclusion Compounds 3, 5, 11, 12 and 15 are isolated from G. vulgaris for the first time. Compound 2, 4, 13, and 16 are isolated from the plant of genus for the first time.
ABSTRACT
Quercetin, a flavonol, has been reported to exhibit a wide range of biological properties including anti-oxidant and anti-inflammatory activities. However, pharmacological properties of quercetin-3-O-β-D-glucuronide (QG), a glycoside derivative of quercetin, have not been extensively examined. The objective of this study is to elucidate the anti-inflammatory property and underlying mechanism of QG in lipopolysaccharide (LPS)-challenged RAW264.7 macrophage cells in comparison with quercetin. QG significantly suppressed LPS-induced extracellular secretion of pro-inflammatory mediators such as nitric oxide (NO) and PGE2, and pro-inflammatory protein expressions of iNOS and COX-2. To elucidate the underlying mechanism of the anti-inflammatory property of QG, involvement of MAPK signaling pathways was examined. QG significantly attenuated LPS-induced activation of JNK and ERK in concentration-dependent manners with a negligible effect on p38. In conclusion, the present study demonstrates QG exerts anti-inflammatory activity through the suppression of JNK and ERK signaling pathways in LPS-challenged RAW264.7 macrophage cells.
Subject(s)
Dinoprostone , Macrophages , Nitric Oxide , Phosphorylation , QuercetinABSTRACT
The effects of quercetin-3-O-β-D-glucuronide (Q3GA)on the triglyceride metabolism and oxidative stress in steatotic HepG2 cells and the underlying mechanism were investigated in this study.Significant fat accu-mulation was documented by Oil Red O staining;intracellular triglyceride levels were detected by triglyceride(TG)enzymatic assay.DCFH-DA staining assay was performed to observe reactive oxygen species (ROS)pro-duction of HepG2 cells.The level of malondialdehyde(MDA)and superoxide dismutase(SOD)were assayed by thibabituric acid method and xanthine oxidase method.Changes in the mRNA expression of peroxisome prolifera-tor-activated receptorα(PPARα);carnitine palmitoyltransferase 1 A(CPT1 A);medium chain acyl-CoA dehydro-genase (MCAD);cytochrome P450 4A11(CYP4A11)and acyl-CoA oxidase(ACO);which are related with fatty acid oxidation were assessed by RT-PCR.Our results showed that Q3GA obviously reduced fat deposition and TG content.At the same time;Q3 GA decreased MDA content and significantly increased the SOD activity with reduced ROS production.Moreover;the PPARα;CPT1A;MCAD expression-related fatty acid βoxidation was upregulated with the treament of Q3GA;while without any change of the expression of CYP4A11;ACO.In conclu-sion;Q3GA prevents FFA-induced HepG2 cell steatosis;and enhances mitochondrial fatty acidβoxidation;which may partly be related to its anti-oxidation ability.