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21 August 2019 : Laboratory Research  

Leonurine Exerts Anti-Catabolic and Anti-Apoptotic Effects via Nuclear Factor kappa B (NF-κB) and Mitogen-Activated Protein Kinase (MAPK) Signaling Pathways in Chondrocytes

Peng-Fei Hu1ABCG, Fang-Fang Sun2ABCDEF, Jing Qian3ACDE*

DOI: 10.12659/MSM.916039

Med Sci Monit 2019; 25:6271-6280


BACKGROUND: Leonurine confers neuroprotection, inhibits myocardial apoptosis, ameliorates endothelial dysfunction, and shows anti-inflammatory effects, and may be beneficial for clinical applications. However, the effects of leonurine on chondrocytes remain unknown. Here, we investigated the protective role of leonurine in rat chondrocytes.

MATERIAL AND METHODS: To explore the potential therapeutic effect of leonurine against osteoarthritis (OA), rat chondrocytes were treated with IL-1β along with different concentrations of leonurine in vitro. The levels of matrix metalloproteinases (MMPs), ADAMTS, Bax, and Bcl-2 were measured by PCR, ELISA, and Western blotting. Caspase-3 activity in chondrocytes was determined using a caspase-3 activity assay. Western blotting was also performed to examine activation of the NF-κB and mitogen-activated protein kinase (MAPK) pathways to elucidate the likely regulatory mechanisms.

RESULTS: Leonurine counteracted IL-1β-induced production of MMP-1, MMP-13, ADAMTS-4, and ADAMTS-5. Leonurine treatment reduced both the mRNA and protein levels of Bax and increased the level of Bcl-2. Leonurine also inhibited the activity of caspase-3 in IL-1β-induced chondrocytes. Furthermore, the activation of MAPK and phosphorylation of p65 were suppressed by leonurine.

CONCLUSIONS: The results of this study indicate that leonurine exerts anti-catabolic and anti-apoptotic effects in chondrocytes in vitro via suppression of the NF-κB and MAPK signaling pathways.

Keywords: Matrix Metalloproteinases, Mitogen-Activated Protein Kinase Phosphatases, NF-kappa B, Osteoarthritis, ADAM Proteins, Apoptosis, Cells, Cultured, Chondrocytes, Gallic Acid, Mitogen-Activated Protein Kinases, Phosphorylation, Signal Transduction


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Medical Science Monitor Basic Research eISSN: 2325-4416
Medical Science Monitor Basic Research eISSN: 2325-4416