Lycopene inhibits IL‐1β‐induced inflammation in mouse chondrocytes and mediates murine osteoarthritis

Zhan, Jingdi; Yan, Zijian; Kong, Xiaojiang; Liu, Junling; Zeng, Lin; Qi, Weihui; Wu, Yifan; Lin, Jian; Pan, Xiaoyun; Xue, Xinghe

doi:10.1111/jcmm.16443

Cited by 20 publications

(13 citation statements)

References 53 publications

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“…Various natural compounds appear to be efficacious in bone-related diseases and hold promise as a succedaneum for synthetic compounds as the next generation of therapeutic agents. Alantolactone and lycopene inhibit IL-1 β -induced activation of NF-κB and Stat3 and attenuate chondrocyte autophagy and extracellular matrix (ECM) degradation ( Pei et al, 2021 ; Zhan et al, 2021 ). Alantolactone at 2 mg/kg alleviated medial meniscus wear and MMP13-positive cell counts in vivo ( Pei et al, 2021 ).…”

Section: Target Signal Transducer and Activator Of Transcription 3 Si...mentioning

confidence: 99%

Stat3 Signaling Pathway: A Future Therapeutic Target for Bone-Related Diseases

Yin

Huang

et al. 2022

Front. Pharmacol.

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Signal transducer and activator of transcription 3 (Stat3) is activated by phosphorylation and translocated to the nucleus to participate in the transcriptional regulation of DNA. Increasing evidences point that aberrant activation or deletion of the Stat3 plays a critical role in a broad range of pathological processes including immune escape, tumorigenesis, and inflammation. In the bone microenvironment, Stat3 acts as a common downstream response protein for multiple cytokines and is engaged in the modulation of cellular proliferation and intercellular interactions. Stat3 has direct impacts on disease progression by regulating mesenchymal stem cells differentiation, osteoclast activation, macrophage polarization, angiogenesis, and cartilage degradation. Here, we describe the theoretical basis and key roles of Stat3 in different bone-related diseases in combination with in vitro experiments and animal models. Then, we summarize and categorize the drugs that target Stat3, providing potential therapeutic strategies for their use in bone-related diseases. In conclusion, Stat3 could be a future target for bone-related diseases.

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Section: Target Signal Transducer and Activator Of Transcription 3 Si...mentioning

confidence: 99%

Stat3 Signaling Pathway: A Future Therapeutic Target for Bone-Related Diseases

Yin

Huang

et al. 2022

Front. Pharmacol.

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“…A recent report demonstrated that an increase in Nrf2 levels can prevent OA progression in rats by inhibiting the NF-κB pathway [ 22 ]. In another study, a treatment strategy that focused on the Nrf2/HO-1 pathway reduced inflammation and cartilage degradation in OA patients, providing a breakthrough for OA treatment [ 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

Carnosine Alleviates Knee Osteoarthritis and Promotes Synoviocyte Protection via Activating the Nrf2/HO-1 Signaling Pathway: An In-Vivo and In-Vitro Study

et al. 2022

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The most common joint disease in the elderly is knee osteoarthritis (OA). It is distinguished by cartilage degradation, subchondral bone loss, and a decrease in joint space. We studied the effects of carnosine (CA) on knee OA in male Wistar rats. OA is induced by anterior cruciate ligament transection combined with medial meniscectomy (ACLT+MMx) method and in vitro studies are conducted in fibroblast-like synoviocyte cells (FLS). The pain was assessed using weight-bearing and paw-withdrawal tests. CA supplementation significantly reduced pain. The enzyme-linked immunosorbent assay (ELISA) method was used to detect inflammatory proteins in the blood and intra-articular synovial fluid (IASF), and CA reduced the levels of inflammatory proteins. Histopathological studies were performed on knee-tissue samples using toluidine blue and hematoxylin and eosin (H and E) assays. CA treatment improved synovial protection and decreased cartilage degradation while decreasing zonal depth lesions. Furthermore, Western blotting studies revealed that the CA-treated group activated nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase (HO-1) and reduced the expression of cyclooxygenase-2 (COX-2). FLS cells were isolated from the knee joints and treated with IL-1β to stimulate the inflammatory response and increase reactive oxygen species (ROS). The matrix metalloproteinase protein (MMP’s) levels (MMP-3, and MMP-13) were determined using the reverse transcription-polymerase chain reaction (RT-PCR), and CA treatment reduced the MMP’s expression levels. When tested using the 2′,7′-dicholorodihydrofluroscene diacetate (DCFDA) assay and the 5,5′,6,6′-tetracholoro-1,1′,3,3′-tertraethylbenzimidazolcarboc janine iodide (JC-1) assay in augmented ROS FLS cells, CA reduced the ROS levels and improved the mitochondrial membrane permeability. This study’s investigation suggests that CA significantly alleviates knee OA both in vitro and in vivo.

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“…Other in vitro and in vivo evidence supports the contribution of proteasome activity to cartilage damage and OA progression [ 25 , 26 , 27 , 28 ].…”

Section: Resultsmentioning

confidence: 84%

“…Accordingly, MG132 has been shown to protect cartilage against the effects of inflammatory mediators by regulating MMP [ 26 ], antioxidant defense [ 27 ], and cartilage markers [ 28 ].…”

Section: Resultsmentioning

confidence: 99%

Dynamics of Connexin 43 Down Modulation in Human Articular Chondrocytes Stimulated by Tumor Necrosis Factor Alpha

Morte

Niada

Giannasi

et al. 2022

IJMS

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Connexin 43 (Cx43) exerts pivotal functions in articular chondrocytes (CH). It is involved in the communication among cells and between cells and the extracellular environment, and it contributes to the maintenance of the correct cell phenotype. The pro-inflammatory cytokine TNFα induces a reduction in Cx43 expression in CH. Here, we studied the dynamics of this decrease in expression. We evaluated Cx43 protein and gene expression and the involvement of C-terminal domain (CTD) cleavage and proteasomal degradation. Treatments able to counteract TNFα action were also examined, together with Gap Junction (GJ) functionality and Cx43 localization. TNFα induced a significant reduction in Cx43 expression already at day 1, and the down modulation reached a peak at day 3 (−46%). The decrease was linked to neither gene expression modulation nor CTD cleavage. Differently, the proteasome inhibitor MG132 reverted TNFα effect, indicating the involvement of proteasomal degradation in Cx43 reduction. In addition, the co-treatment with the anabolic factor TGF-β1 restored Cx43 levels. Cx43 decrease occurred both at the membrane level, where it partially influenced GJ communication, and in the nucleus. In conclusion, TNFα induced a rapid and lasting reduction in Cx43 expression mostly via the proteasome. The down modulation could be reverted by cartilage-protective factors such as MG132 and TGF-β1. These findings suggest a possible involvement of Cx43 perturbation during joint inflammation.

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Lycopene inhibits IL‐1β‐induced inflammation in mouse chondrocytes and mediates murine osteoarthritis

Cited by 20 publications

References 53 publications

Stat3 Signaling Pathway: A Future Therapeutic Target for Bone-Related Diseases

Stat3 Signaling Pathway: A Future Therapeutic Target for Bone-Related Diseases

Carnosine Alleviates Knee Osteoarthritis and Promotes Synoviocyte Protection via Activating the Nrf2/HO-1 Signaling Pathway: An In-Vivo and In-Vitro Study

Dynamics of Connexin 43 Down Modulation in Human Articular Chondrocytes Stimulated by Tumor Necrosis Factor Alpha

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