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The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway
OBJECTIVES: To explore the role of medial collateral ligament repair in knee osteoarthritis based on TLR4/MyD88/NF-κ inflammatory signaling pathway. METHODS: The modified Hulth method was used to establish models, which were divided into a repair group, a model group, and a sham operation group. The...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Society of Musculoskeletal and Neuronal Interactions
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493448/ https://www.ncbi.nlm.nih.gov/pubmed/32877976 |
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author | Li, Zhiyong Zou, Yu Fan, Dandan Zhang, Wenlong Gao, Hongwei Ge, Na Tian, Shaohua |
author_facet | Li, Zhiyong Zou, Yu Fan, Dandan Zhang, Wenlong Gao, Hongwei Ge, Na Tian, Shaohua |
author_sort | Li, Zhiyong |
collection | PubMed |
description | OBJECTIVES: To explore the role of medial collateral ligament repair in knee osteoarthritis based on TLR4/MyD88/NF-κ inflammatory signaling pathway. METHODS: The modified Hulth method was used to establish models, which were divided into a repair group, a model group, and a sham operation group. The repair group was treated with medial ligament repair technology. Synovium and cartilage morphological changes were evaluated by hematoxylin-eosin staining to determine the degree of reparation. The cartilage was evaluated by the Mankin’s score, and inflammatory factors in cartilage tissues were determined by ELISA. The changes in TLR4, MyD88, and NF-κB levels were analyzed using the real-time quantitative PCR and Western blot assays. RESULTS: The synovial and cartilage damages in the repair group and the sham operation group were significantly alleviated compared to the model group. The Mankin’s score of the model group was significantly lower than the other two groups. The expression of inflammatory factors in the repair group and the sham operation group were significantly lower than in the model group. The expressions of those factors in the repair group and the model group were higher than those in the model group. CONCLUSIONS: Medial ligament repair can improve the cartilage morphology and delay the development and progression of knee osteoarthritis by inhibiting the TLR4/MyD88/NF-κB signaling pathway. |
format | Online Article Text |
id | pubmed-7493448 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | International Society of Musculoskeletal and Neuronal Interactions |
record_format | MEDLINE/PubMed |
spelling | pubmed-74934482020-09-21 The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway Li, Zhiyong Zou, Yu Fan, Dandan Zhang, Wenlong Gao, Hongwei Ge, Na Tian, Shaohua J Musculoskelet Neuronal Interact Original Article OBJECTIVES: To explore the role of medial collateral ligament repair in knee osteoarthritis based on TLR4/MyD88/NF-κ inflammatory signaling pathway. METHODS: The modified Hulth method was used to establish models, which were divided into a repair group, a model group, and a sham operation group. The repair group was treated with medial ligament repair technology. Synovium and cartilage morphological changes were evaluated by hematoxylin-eosin staining to determine the degree of reparation. The cartilage was evaluated by the Mankin’s score, and inflammatory factors in cartilage tissues were determined by ELISA. The changes in TLR4, MyD88, and NF-κB levels were analyzed using the real-time quantitative PCR and Western blot assays. RESULTS: The synovial and cartilage damages in the repair group and the sham operation group were significantly alleviated compared to the model group. The Mankin’s score of the model group was significantly lower than the other two groups. The expression of inflammatory factors in the repair group and the sham operation group were significantly lower than in the model group. The expressions of those factors in the repair group and the model group were higher than those in the model group. CONCLUSIONS: Medial ligament repair can improve the cartilage morphology and delay the development and progression of knee osteoarthritis by inhibiting the TLR4/MyD88/NF-κB signaling pathway. International Society of Musculoskeletal and Neuronal Interactions 2020 /pmc/articles/PMC7493448/ /pubmed/32877976 Text en Copyright: © Journal of Musculoskeletal and Neuronal Interactions http://creativecommons.org/licenses/by-nc-sa/4.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 4.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Li, Zhiyong Zou, Yu Fan, Dandan Zhang, Wenlong Gao, Hongwei Ge, Na Tian, Shaohua The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway |
title | The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway |
title_full | The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway |
title_fullStr | The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway |
title_full_unstemmed | The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway |
title_short | The mechanism of medial collateral ligament repair in knee osteoarthritis based on the TLR4/MyD88/NF-κB inflammatory signaling pathway |
title_sort | mechanism of medial collateral ligament repair in knee osteoarthritis based on the tlr4/myd88/nf-κb inflammatory signaling pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7493448/ https://www.ncbi.nlm.nih.gov/pubmed/32877976 |
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