1. Academic Validation
  2. Galangin attenuates IL-1β-induced catabolism in mouse chondrocytes and ameliorates murine osteoarthritis

Galangin attenuates IL-1β-induced catabolism in mouse chondrocytes and ameliorates murine osteoarthritis

  • Am J Transl Res. 2021 Aug 15;13(8):8742-8753.
Yanben Wang 1 2 Tan Zhang 1 Qichang Yang 1 3 Yewei Jia 1 Peng Sun 1 3 Ziyuan Fu 1 2 Weiqi Han 1 Yu Qian 1
Affiliations

Affiliations

  • 1 Department of Orthopaedics, Shaoxing Hospital, Zhejiang University School of Medicine Shaoxing, Zhejiang, China.
  • 2 Department of Orthopaedics, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University Hangzhou, Zhejiang, China.
  • 3 The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University Wenzhou, Zhejiang, China.
PMID: 34539991
Abstract

Objective: Osteoarthritis (OA) is one of the most common chronic diseases, which is characterized by cartilage degeneration, subchondral osteosclerosis, and synovitis. Accumulating evidence has shown that galangin, a flavonoid derived from medicinal herbs, exhibits numerous pharmacological activities in various diseases. This study aimed to investigate the effects of galangin on interleukin (IL)-1β-induced inflammation in mouse chondrocytes and explore the underlying mechanisms.

Methods: In this study, we investigated the protective effects of galangin on IL-1β-induced inflammatory response in vitro using the CCK-8 assay, RT-qPCR, western blotting, and immunofluorescence staining. In addition, the therapeutic effects of galangin on the anterior cruciate ligament transection (ACLT) mouse model were also explored in vivo. Results: Galangin treatment suppressed the expression of IL-1β-induced inflammatory cytokines, such as nitric oxide synthase, cyclooxygenase-2, TNF-α, and IL-6. Furthermore, galangin attenuated hypertrophic conversion and the extracellular matrix degradation via inhibiting the expression of catabolic enzymes. Mechanistically, galangin inhibited the activation of the JNK and ERK MAPK pathways and nuclear factor kappa-B (NF-κB) signaling pathway. In addition, galangin treatment ameliorated cartilage degeneration in an OA model in vivo. Conclusion: Galangin suppressed the IL-β-induced inflammatory response in vitro and ameliorated cartilage degeneration in vivo via inhibiting the NF-κB pathway and JNK and ERK pathways, suggesting its potential as an effective candidate for the treatment of OA.

Keywords

Galangin; IL-1β; NF-κB; chondrocyt; osteoarthritis.

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