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Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway

CONTEXT: The prevalence of gout has greatly increased, and it has become the most common inflammatory arthritis in men. Isovitexin possesses anti-inflammatory and antioxidant properties. OBJECTIVE: We explored the effects of isovitexin on rats with acute gouty arthritis (GA). MATERIALS AND METHODS:...

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Autores principales: Sun, Xiujiang, Li, Peng, Qu, Xiaoyi, Liu, Wenguang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8480722/
https://www.ncbi.nlm.nih.gov/pubmed/34582722
http://dx.doi.org/10.1080/13880209.2021.1979595
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author Sun, Xiujiang
Li, Peng
Qu, Xiaoyi
Liu, Wenguang
author_facet Sun, Xiujiang
Li, Peng
Qu, Xiaoyi
Liu, Wenguang
author_sort Sun, Xiujiang
collection PubMed
description CONTEXT: The prevalence of gout has greatly increased, and it has become the most common inflammatory arthritis in men. Isovitexin possesses anti-inflammatory and antioxidant properties. OBJECTIVE: We explored the effects of isovitexin on rats with acute gouty arthritis (GA). MATERIALS AND METHODS: Fifty-four Sprague-Dawley rats were assigned to five groups: sham, model, positive (colchicine, 0.3 mg/kg), isovitexin (100 mg/kg), TLR4 inhibitor (TAK-242, 3 mg/kg) and isovitexin + TAK-242. The gait of rats and the ankle joint swelling index were monitored. The levels of tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6, and pathological changes in the synovial tissues were determined. RESULTS: Isovitexin significantly reduced the ankle joint swelling index at day 7 compared to that in the model group (4.39 ± 1.01 vs. 6.09 ± 1.31). Moreover, isovitexin alleviated the infiltration of inflammatory cells and ameliorated the proliferation of synovial cells. The levels of TNF-α (93.42 ± 5.02 pg/mL), IL-1β (25.46 ± 1.91 pg/mL) and IL-6 (194.71 ± 7.92 pg/mL) in the isovitexin group were significantly lower than in the model group (129.39 ± 5.43, 39.60 ± 2.71 and 223.77 ± 5.35 pg/mL). The expression of TLR4, MyD88 and p-NF-κB-p65 was remarkably decreased after isovitexin and colchicine treatment. The effect of isovitexin was similar to that colchicine. Furthermore, the combination of isovitexin and TAK-242 had better effect, and there was no significantly difference with colchicine treatment. DISCUSSION AND CONCLUSIONS: Isovitexin ameliorates joint inflammation in acute GA via the TLR4/MyD88/NF-κB pathway. Isovitexin may be a potential substitute medicine for GA.
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spelling pubmed-84807222021-09-30 Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway Sun, Xiujiang Li, Peng Qu, Xiaoyi Liu, Wenguang Pharm Biol Research Article CONTEXT: The prevalence of gout has greatly increased, and it has become the most common inflammatory arthritis in men. Isovitexin possesses anti-inflammatory and antioxidant properties. OBJECTIVE: We explored the effects of isovitexin on rats with acute gouty arthritis (GA). MATERIALS AND METHODS: Fifty-four Sprague-Dawley rats were assigned to five groups: sham, model, positive (colchicine, 0.3 mg/kg), isovitexin (100 mg/kg), TLR4 inhibitor (TAK-242, 3 mg/kg) and isovitexin + TAK-242. The gait of rats and the ankle joint swelling index were monitored. The levels of tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6, and pathological changes in the synovial tissues were determined. RESULTS: Isovitexin significantly reduced the ankle joint swelling index at day 7 compared to that in the model group (4.39 ± 1.01 vs. 6.09 ± 1.31). Moreover, isovitexin alleviated the infiltration of inflammatory cells and ameliorated the proliferation of synovial cells. The levels of TNF-α (93.42 ± 5.02 pg/mL), IL-1β (25.46 ± 1.91 pg/mL) and IL-6 (194.71 ± 7.92 pg/mL) in the isovitexin group were significantly lower than in the model group (129.39 ± 5.43, 39.60 ± 2.71 and 223.77 ± 5.35 pg/mL). The expression of TLR4, MyD88 and p-NF-κB-p65 was remarkably decreased after isovitexin and colchicine treatment. The effect of isovitexin was similar to that colchicine. Furthermore, the combination of isovitexin and TAK-242 had better effect, and there was no significantly difference with colchicine treatment. DISCUSSION AND CONCLUSIONS: Isovitexin ameliorates joint inflammation in acute GA via the TLR4/MyD88/NF-κB pathway. Isovitexin may be a potential substitute medicine for GA. Taylor & Francis 2021-09-28 /pmc/articles/PMC8480722/ /pubmed/34582722 http://dx.doi.org/10.1080/13880209.2021.1979595 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Sun, Xiujiang
Li, Peng
Qu, Xiaoyi
Liu, Wenguang
Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway
title Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway
title_full Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway
title_fullStr Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway
title_full_unstemmed Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway
title_short Isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway
title_sort isovitexin alleviates acute gouty arthritis in rats by inhibiting inflammation via the tlr4/myd88/nf-κb pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8480722/
https://www.ncbi.nlm.nih.gov/pubmed/34582722
http://dx.doi.org/10.1080/13880209.2021.1979595
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