Urolithin a attenuates IL-1β-induced inflammatory responses and cartilage degradation via inhibiting the MAPK/NF-κB signaling pathways in rat articular chondrocytes

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Abstract

Background

Osteoarthritis (OA) is characterized by inflammation and extracellular matrix (ECM) degradation and is one of the most common chronic degenerative joint diseases that causes pain and disability in adults. Urolithin A (UA) has been widely reported for its anti-inflammatory properties in several chronic diseases. However, the effects of UA on OA remain unclear. The aim of the current study was to investigate the anti-inflammatory effects and mechanism of UA in interleukin-1β (IL-1β)-induced chondrocytes.

Results

No marked UA cytotoxicity was noted, and UA protected cartilage from damage following IL-1β stimulation in micromasses. Moreover, UA promoted the expression of anabolic factors including Sox-9, Collagen II, and Aggrecan while inhibiting the expression of catabolic factors such as matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS-4) in rat chondrocytes. Protective effects of UA were also observed in ex vivo organ culture of articular cartilage. Mechanistically, IL-1β significantly activated and upregulated the expression of p-ERK 1/2, p-JNK, p-P38, and p-P65, while UA protected chondrocytes against IL-1β-induced injury by activating the mitogen-activated kinase (MAPK)/nuclear factor-κB (NF-κB) signaling pathways.

Conclusion

Our results provide the evidence that UA could attenuate IL-1β-induced cell injury in chondrocytes via its anti-inflammatory action. UA may be a promising therapeutic agent in the treatment of OA.

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Most cited references 28

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Osteoarthritis cartilage histopathology: grading and staging.

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Current osteoarthritis (OA) histopathology assessment methods have difficulties in their utility for early disease, as well as their reproducibility and validity. Our objective was to devise a more useful method to assess OA histopathology that would have wide application for clinical and experimental OA assessment and would become recognized as the standard method. An OARSI Working Group deliberated on principles, standards and features for an OA cartilage pathology assessment system. Using current knowledge of the pathophysiology of OA morphologic features, a proposed system was presented at OARSI 2000. Subsequently, this was widely circulated for comments amongst experts in OA pathology. An OA cartilage pathology assessment system based on six grades, which reflect depth of the lesion and four stages reflecting extent of OA over the joint surface was developed. The OARSI cartilage OA histopathology grading system appears consistent and simple to apply. Further studies are required to confirm the system's utility.

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The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon.

Dallas R Donohoe, Nikhil Garge, Xinxin Zhang … (2011)

The microbiome is being characterized by large-scale sequencing efforts, yet it is not known whether it regulates host metabolism in a general versus tissue-specific manner or which bacterial metabolites are important. Here, we demonstrate that microbiota have a strong effect on energy homeostasis in the colon compared to other tissues. This tissue specificity is due to colonocytes utilizing bacterially produced butyrate as their primary energy source. Colonocytes from germfree mice are in an energy-deprived state and exhibit decreased expression of enzymes that catalyze key steps in intermediary metabolism including the TCA cycle. Consequently, there is a marked decrease in NADH/NAD(+), oxidative phosphorylation, and ATP levels, which results in AMPK activation, p27(kip1) phosphorylation, and autophagy. When butyrate is added to germfree colonocytes, it rescues their deficit in mitochondrial respiration and prevents them from undergoing autophagy. The mechanism is due to butyrate acting as an energy source rather than as an HDAC inhibitor. Copyright © 2011 Elsevier Inc. All rights reserved.

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Osteoarthritis.

Mary Goldring, Steven R Goldring (2007)

Osteoarthritis (OA) is characterized by degeneration of articular cartilage, limited intraarticular inflammation with synovitis, and changes in peri-articular and subchondral bone. Multiple factors are involved in the pathogenesis of OA, including mechanical influences, the effects of aging on cartilage matrix composition and structure, and genetic factors. Since the initial stages of OA involve increased cell proliferation and synthesis of matrix proteins, proteinases, growth factors, cytokines, and other inflammatory mediators by chondrocytes, research has focused on the chondrocyte as the cellular mediator of OA pathogenesis. The other cells and tissues of the joint, including the synovium and subchondral bone, also contribute to pathogenesis. The adult articular chondrocyte, which normally maintains the cartilage with a low turnover of matrix constituents, has limited capacity to regenerate the original cartilage matrix architecture. It may attempt to recapitulate phenotypes of early stages of cartilage development, but the precise zonal variations of the original cartilage cannot be replicated. Current pharmacological interventions that address chronic pain are insufficient, and no proven structure-modifying therapy is available. Cartilage tissue engineering with or without gene therapy is the subject of intense investigation. There are multiple animal models of OA, but there is no single model that faithfully replicates the human disease. This review will focus on questions currently under study that may lead to better understanding of mechanisms of OA pathogenesis and elucidation of effective strategies for therapy, with emphasis on mechanisms that affect the function of chondrocytes and interactions with surrounding tissues. 2007 Wiley-Liss, Inc.

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Author and article information

Contributors

Sheng-long Ding:

ORCID: https://orcid.org/0000-0003-0682-3596

dslong05@outlook.com

Zhi-ying Pang: adampang0126@gmail.com

Xue-mei Chen: cxm0918@outlook.com

Zheng Li: 17111210053@fudan.edu.cn

Xin-xin Liu: 17211210060@fudan.edu.cn

Qi-lin Zhai: zhaiql@163.com

Jun-ming Huang: mhyper@sina.com

Zhi-yong Ruan: xyrzy818@163.com

Journal

Journal ID (nlm-ta): J Inflamm (Lond)

Journal ID (iso-abbrev): J Inflamm (Lond)

Title: Journal of Inflammation (London, England)

Publisher: BioMed Central (London )

ISSN (Electronic): 1476-9255

Publication date (Electronic): 24 March 2020

Publication date PMC-release: 24 March 2020

Publication date Collection: 2020

Volume: 17

Electronic Location Identifier: 13

Affiliations

[1 ]GRID grid.8547.e, ISNI 0000 0001 0125 2443, Department of Orthopaedic Surgery, Qingpu Branch of Zhongshan Hospital, , Fudan University, ; 1158 Gong Yuan Dong Road, Qingpu District, Shanghai, 201700 China

[2 ]GRID grid.8547.e, ISNI 0000 0001 0125 2443, Department of Orthopaedic Surgery, Zhongshan Hospital, , Fudan University, ; 180 Feng Lin Road, Xuhui District, Shanghai, 200032 China

[3 ]GRID grid.412528.8, ISNI 0000 0004 1798 5117, Department of Anesthesiology, , Shanghai JiaoTong University Affiliated Shanghai Sixth People’s Hospital, ; Shanghai, 200233 China

Author information

Sheng-long Ding https://orcid.org/0000-0003-0682-3596

Article

Publisher ID: 242

DOI: 10.1186/s12950-020-00242-8

PMC ID: 7092521

PubMed ID: 32210738

SO-VID: a233993a-bb1f-49af-81ca-8273126b1b6c

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 30 October 2019

Date accepted : 13 March 2020

Funding

Funded by: Project of Qingpu District Science and Technology Commission

Award ID: QKY2018-11

Award Recipient : Zhi-yong Ruan

Funded by: the Project of Qingpu Branch of Zhongshan Hospital

Award ID: QYZ2019-02 and QY2019-04

Award Recipient : Zhi-yong Ruan

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ScienceOpen disciplines: Immunology

Keywords: urolithin a,osteoarthritis,nf-κb,mapk,inflammation

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ScienceOpen disciplines: Immunology

Keywords: urolithin a, osteoarthritis, nf-κb, mapk, inflammation

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Urolithin a attenuates IL-1β-induced inflammatory responses and cartilage degradation via inhibiting the MAPK/NF-κB signaling pathways in rat articular chondrocytes

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Most cited references 28

Osteoarthritis cartilage histopathology: grading and staging.

The microbiome and butyrate regulate energy metabolism and autophagy in the mammalian colon.

Osteoarthritis.

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