The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways
Gouty arthritis (GA) is a frequent inflammatory disease characterized by pain, swelling, and stiffness of joints. Neoastilbin is a flavonoid isolated from the rhizome of <i>Smilax glabra</i>, which possesses various anti-inflammatory effects. However, the mechanism of neoastilbin in trea...
Main Authors: | , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2022-05-01
|
Series: | Molecules |
Subjects: | |
Online Access: | https://www.mdpi.com/1420-3049/27/11/3477 |
_version_ | 1797492467719733248 |
---|---|
author | Wenjing Xu Fenfen Li Xiaoxi Zhang Chenxi Wu Yan Wang Yanjing Yao Daozong Xia |
author_facet | Wenjing Xu Fenfen Li Xiaoxi Zhang Chenxi Wu Yan Wang Yanjing Yao Daozong Xia |
author_sort | Wenjing Xu |
collection | DOAJ |
description | Gouty arthritis (GA) is a frequent inflammatory disease characterized by pain, swelling, and stiffness of joints. Neoastilbin is a flavonoid isolated from the rhizome of <i>Smilax glabra</i>, which possesses various anti-inflammatory effects. However, the mechanism of neoastilbin in treating GA has not yet been clarified. Thus, this study was to investigate the protective effects of neoastilbin in both monosodium urate (MSU) stimulated THP-1-derived macrophages and the animal model of GA by injecting MSU into the ankle joints of mice. The levels of key inflammatory cytokines in MSU stimulated THP-1-derived macrophages were detected by enzyme-linked immunosorbent assay (ELISA) kits. Protein expressions of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasome pathways were further detected by Western blotting. In addition, swelling degree of ankle joints, the levels of inflammatory factors, infiltration of inflammatory cells and the expressions of related proteins were determined. Swelling degree and histopathological injury in ankle joints of MSU-injected mice were significantly decreased after being treated with neoastilbin. Moreover, neoastilbin significantly diminished the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), suppressing the activation of NF-κB and NLRP3 inflammasome pathways in both MSU stimulated THP-1-derived macrophages and the mouse model of GA. In summary, neoastilbin could alleviate GA by inhibiting the NF-κB and NLRP3 inflammasome pathways, which provided some evidence for neoastilbin as a promising therapeutic agent for GA treatment. |
first_indexed | 2024-03-10T01:04:05Z |
format | Article |
id | doaj.art-01e8b00a0e404292b5fad9c5a6665d65 |
institution | Directory Open Access Journal |
issn | 1420-3049 |
language | English |
last_indexed | 2024-03-10T01:04:05Z |
publishDate | 2022-05-01 |
publisher | MDPI AG |
record_format | Article |
series | Molecules |
spelling | doaj.art-01e8b00a0e404292b5fad9c5a6665d652023-11-23T14:29:22ZengMDPI AGMolecules1420-30492022-05-012711347710.3390/molecules27113477The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome PathwaysWenjing Xu0Fenfen Li1Xiaoxi Zhang2Chenxi Wu3Yan Wang4Yanjing Yao5Daozong Xia6School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaAcademy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaSchool of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, ChinaGouty arthritis (GA) is a frequent inflammatory disease characterized by pain, swelling, and stiffness of joints. Neoastilbin is a flavonoid isolated from the rhizome of <i>Smilax glabra</i>, which possesses various anti-inflammatory effects. However, the mechanism of neoastilbin in treating GA has not yet been clarified. Thus, this study was to investigate the protective effects of neoastilbin in both monosodium urate (MSU) stimulated THP-1-derived macrophages and the animal model of GA by injecting MSU into the ankle joints of mice. The levels of key inflammatory cytokines in MSU stimulated THP-1-derived macrophages were detected by enzyme-linked immunosorbent assay (ELISA) kits. Protein expressions of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasome pathways were further detected by Western blotting. In addition, swelling degree of ankle joints, the levels of inflammatory factors, infiltration of inflammatory cells and the expressions of related proteins were determined. Swelling degree and histopathological injury in ankle joints of MSU-injected mice were significantly decreased after being treated with neoastilbin. Moreover, neoastilbin significantly diminished the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), suppressing the activation of NF-κB and NLRP3 inflammasome pathways in both MSU stimulated THP-1-derived macrophages and the mouse model of GA. In summary, neoastilbin could alleviate GA by inhibiting the NF-κB and NLRP3 inflammasome pathways, which provided some evidence for neoastilbin as a promising therapeutic agent for GA treatment.https://www.mdpi.com/1420-3049/27/11/3477gouty arthritisneoastilbinNLRP3 inflammasomeNF-κB pathway |
spellingShingle | Wenjing Xu Fenfen Li Xiaoxi Zhang Chenxi Wu Yan Wang Yanjing Yao Daozong Xia The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways Molecules gouty arthritis neoastilbin NLRP3 inflammasome NF-κB pathway |
title | The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways |
title_full | The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways |
title_fullStr | The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways |
title_full_unstemmed | The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways |
title_short | The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways |
title_sort | protective effects of neoastilbin on monosodium urate stimulated thp 1 derived macrophages and gouty arthritis in mice through nf κb and nlrp3 inflammasome pathways |
topic | gouty arthritis neoastilbin NLRP3 inflammasome NF-κB pathway |
url | https://www.mdpi.com/1420-3049/27/11/3477 |
work_keys_str_mv | AT wenjingxu theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT fenfenli theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT xiaoxizhang theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT chenxiwu theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT yanwang theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT yanjingyao theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT daozongxia theprotectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT wenjingxu protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT fenfenli protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT xiaoxizhang protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT chenxiwu protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT yanwang protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT yanjingyao protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways AT daozongxia protectiveeffectsofneoastilbinonmonosodiumuratestimulatedthp1derivedmacrophagesandgoutyarthritisinmicethroughnfkbandnlrp3inflammasomepathways |