Calcitonin protects rat chondrocytes from IL‑1β injury via the Wnt/β‑catenin pathway

Bai, Mingxiao; Liu, Ge; Chen, Hui; Jin, Qunhua

doi:10.3892/etm.2019.7806

Cited by 7 publications

(9 citation statements)

References 17 publications

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“…IL-1β is the main contributor to OA pathology and commonly used as an inducer in in vitro inflammatory model of chondrocyte [22]. In line with previous report [3,23], IL-1β treatment significantly decreased the cell viability of mouse chondrocyte in a time-dependent manner (Fig. 1b).…”

Section: Ligusticum Wallichii Extracts Protect Mouse Chondrocytes Agasupporting

confidence: 88%

“…Osteoarthritis (OA), a chronic and degenerative joint disease that is appreciated to involve low-grade inflammation and characterizes by the progressive deterioration of articular cartilage, osteophyte formation, subchondral sclerosis, matrix degradation and matrix synthesis imbalance, is one of the most expensive and disabling forms of arthritis, being more widespread than rheumatoid arthritis or other arthritic diseases and representing a major burden of public health [1][2][3][4]. In OA, this low-grade inflammation causes a hypoxia condition and resulting metabolic shift in energy metabolism from a resting regulatory state to an extremely metabolically active state to sustain energy homeostasis and promote cell survival, thereby confining the metabolism of pyruvate by the citrate cycle in mitochondria during oxidative phosphorylation and impacting the metabolic flow of chondrocytes and other cells localized in articular cartilage [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

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A metabolic exploration of the protective effect of Ligusticum wallichii on IL-1β-injured mouse chondrocytes

Wei¹,

Dong²,

Guan³

et al. 2020

Chin Med

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Background: Osteoarthritis (OA) is a metabolic disorder and able to be relieved by traditional Chinese medicines. However, the effect of Ligusticum wallichii on OA is unknown. Methods: Cytokine IL-1β and L. wallichii extracts were used to stimulate the primary mouse chondrocytes. MTT assay was used to measure the cell viability. The mRNA and protein level of each gene were test by qRT-PCR and western blotting, respectively. The rate of apoptotic cell was measured by flow cytometry. GC/MS-based metabolomics was utilized to characterize the variation of metabolome. Results: Here, we found that L. wallichii attenuated the IL-1β-induced apoptosis, inflammatory response, and extracellular matrix (ECM) degradation in mouse chondrocytes. Then we used GC/MS-based metabolomics to characterize the variation of metabolomes. The established metabolic profile of mouse chondrocytes showed that the abundance of most metabolites (n = 40) altered by IL-1β stimulation could be repressed by L. wallichii treatment. Multivariate data analysis identified that cholesterol, linoleic acid, hexadecandioic acid, proline, l-valine, l-leucine, pyruvate, palmitic acid, and proline are the most key biomarkers for understanding the metabolic role of L. wallichii in IL-1β-treated chondrocytes. Further pathway analysis using these metabolites enriched fourteen metabolic pathways, which were dramatically changed in IL-1β-treated chondrocytes and capable of being reprogrammed by L. wallichii incubation. These enriched pathways were involved in carbon metabolisms, fatty acid biosynthesis, and amino acid metabolisms. Conclusions: These findings provide potential clues that metabolic strategies are linked to protective mechanisms of L. wallichii treatment in IL-1β-stimulated chondrocytes and emphasize the importance of metabolic strategies against inflammatory responses in OA development.

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Section: Ligusticum Wallichii Extracts Protect Mouse Chondrocytes Agasupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

A metabolic exploration of the protective effect of Ligusticum wallichii on IL-1β-injured mouse chondrocytes

Wei¹,

Dong²,

Guan³

et al. 2020

Chin Med

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“…MMPs and ADAMTSs serve as key players in the degradation of ECM components, contributing to the destruction of articular cartilage (36). Curcumin treatment has been previously demonstrated to inhibit MMP9 and ADAMTS5 in a rat OA model, which was further confirmed in IL-1βinjured chondrocytes (37). This current study demonstrated that curcumin obviously prevented the IL-1β-induced MMP9 and ADAMTS5 expression at the mRNA and protein levels in mouse chondrocytes.…”

Section: Discussionsupporting

confidence: 73%

Curcumin exerts a protective effect on murine knee chondrocytes treated with IL-1β through blocking the NF-κB/HIF-2α signaling pathway

Wang¹,

Ye²,

Wei³

et al. 2021

Ann Transl Med

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Background: Osteoarthritis (OA) is characterized by erosion and degradation of articular cartilage. This study assessed the effects of curcumin on mouse knee cartilage chondrocytes. Methods: Chondrocytes were treated for 24 hours with interleukin IL-1β (10 ng/mL) alone, or the combination of curcumin (10, 20, and 50 μM) and IL-1β. The proliferation, viability, and cytotoxicity of the chondrocytes were evaluated by the MTS assay. Expression of SOX9, AGG, Col2α, MMP9, ADAMTS5, COX2, iNOS, pIκB-α, pNF-κB, and hypoxia-inducible factor-2α (HIF-2α) were detected by western blotting or quantitative polymerase chain reaction (q-PCR). Nuclear translocation of NF-κB and HIF-2α were investigated by immunofluorescence and immunohistochemistry. In in vivo experiments, mice were subjected to destabilization of the medial meniscus (DMM) and given curcumin orally for 6 weeks. Cartilage integrity was evaluated by OARSI (Osteoarthritic Research Society International) scores. Results: Curcumin significantly inhibited the IL-1β-induced reduction of cell viability, degradation of ECM, and the expression of SOX9, Col2α, and AGG (P<0.01). Western blotting, immunofluorescence and immunohistochemistry experiments demonstrated that curcumin dramatically inhibited the activation of NF-κB/HIF-2α in chondrocytes treated with IL-1β (P<0.01). The articular scores were significantly lower in the DMM-induced OA mice compared to OA mice treated with curcumin (P<0.01). Conclusions: Curcumin may have the potential to inhibit OA development, partly through suppressing the activation of the NF-κB/HIF-2α pathway.

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“…Among these inflammatory factors, cells challenged with IL-1β have been widely used to mimic arthritis in in vitro studies. Previous studies have indicated that apoptosis is significantly increased in IL-1β (10 ng/ml)-induced chondrocytes (22,23). Bai et al (22) used different concentrations of IL-1β (0.5, 1.0, 2.5, 5.0, 10.0 and 20.0 ng/ml) to injure chondrocytes and their results suggested that the optimal dose of IL-1β was 10 ng/ml.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have indicated that apoptosis is significantly increased in IL-1β (10 ng/ml)-induced chondrocytes (22,23). Bai et al (22) used different concentrations of IL-1β (0.5, 1.0, 2.5, 5.0, 10.0 and 20.0 ng/ml) to injure chondrocytes and their results suggested that the optimal dose of IL-1β was 10 ng/ml. Therefore, in the present study, an IL-1β concentration of (10 ng/ml) was selected for subsequent experiments.…”

Section: Discussionmentioning

confidence: 99%

Bioinformatics analysis and experimental validation of differentially expressed genes in mouse articular chondrocytes treated with IL‑1β using microarray data

Fan

Peng

et al. 2021

Exp Ther Med

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Osteoarthritis (OA) is the most prevalent chronic degenerative disease that affects the health of the elderly. The present study aimed to identify significant genes involved in OA via bioinformatics analysis. A gene expression dataset (GSE104793) was downloaded from the Gene Expression Omnibus. Bioinformatics analysis was then performed in order to identify differentially expressed genes (DEGs) between untreated chondrocytes and chondrocytes cultured with interleukin-1β (IL-1β) for 24 h. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using Metascape. A protein-protein interaction network of DEGs was constructed using the Search Tool for the Retrieval of Interacting Genes. Gene set enrichment analysis (GSEA) was performed using GSEA software. Furthermore, chondrocytes were extracted and treated with IL-1β (10 ng/ml) for 24 h, and reverse-transcription quantitative PCR was used to confirm differential expression of hub genes. Patient samples were also collected to verify the bioinformatic analysis results. Based on the cut-off criteria used for determination of the DEGs, a total of 844 DEGs, including 498 upregulated and 346 downregulated DEGs, were identified. The DEGs were mainly enriched in the GO terms and KEGG pathways 'inflammatory response', 'negative regulation of cell proliferation', 'ossification', 'taxis', 'blood vessel morphogenesis', 'extracellular structure organization', 'mitotic cell cycle process' and 'TNF signaling pathway'. The majority of the PCR results, namely the differential expression of kininogen 2, complement C3, cyclin B1, cell division cycle 20, cyclin A2, 1-phosphatidylinositol 4-kinase, BUB1 mitotic checkpoint serine/threonine kinase, kinesin family member 11, cyclin B2 and BUB1 mitotic checkpoint serine/threonine kinase B were consistent with the bioinformatics results. Collectively, the present observations provided a regulation network of IL-1β-stimulated chondrocytes, which may provide potential targets of OA therapy.

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Calcitonin protects rat chondrocytes from IL‑1β injury via the Wnt/β‑catenin pathway

Cited by 7 publications

References 17 publications

A metabolic exploration of the protective effect of Ligusticum wallichii on IL-1β-injured mouse chondrocytes

A metabolic exploration of the protective effect of Ligusticum wallichii on IL-1β-injured mouse chondrocytes

Curcumin exerts a protective effect on murine knee chondrocytes treated with IL-1β through blocking the NF-κB/HIF-2α signaling pathway

Bioinformatics analysis and experimental validation of differentially expressed genes in mouse articular chondrocytes treated with IL‑1β using microarray data

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