Green tea polyphenols attenuate LPS-induced inflammation through upregulating microRNA-9 in murine chondrogenic ATDC5

Qiao Zhang1, Yongkun Wang1, Mingran Zhang1

  • 1Department of Orthopaedics, China-Japan Union Hospital of Jilin University, Changchun, Jilin, China.

Abstract

Insights

Green tea polyphenols (GTP) protect against osteoarthritis inflammation by upregulating miR-9, which suppresses key inflammatory pathways like MAPK and NF-κB in ATDC5 cells.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoarthritis (OA) is a widespread chronic musculoskeletal disorder linked to inflammation.
  • There is a critical need for improved therapeutic agents to manage OA outcomes.
  • This study investigates the protective effects of green tea polyphenols (GTP) in an OA model.

Purpose of the Study:

  • To verify the protective role of green tea polyphenols (GTP) in an in vitro osteoarthritis model.
  • To elucidate the regulatory mechanisms underlying GTP's effects on inflammation.
  • To explore the involvement of miR-9 and associated signaling pathways.

Main Methods:

  • ATDC5 cells were stimulated with lipopolysaccharide (LPS) to induce an inflammatory response.
  • Cell viability, apoptosis, protein levels, and pro-inflammatory factors were assessed.
  • miR-9 levels were modulated using mimics and inhibitors, and signaling pathways (MAPK, NF-κB) were analyzed.

Main Results:

  • LPS induced inflammatory damage in ATDC5 cells, characterized by reduced viability and increased apoptosis and cytokine levels.
  • GTP pretreatment significantly mitigated LPS-induced inflammatory damage.
  • GTP enhanced miR-9 levels, which in turn suppressed MAPK and NF-κB pathways, mediating the protective effects.

Conclusions:

  • Green tea polyphenols (GTP) demonstrate a protective effect against LPS-induced inflammation in ATDC5 cells.
  • GTP exerts its anti-inflammatory action by positively regulating miR-9.
  • This miR-9 regulation leads to the suppression of the MAPK and NF-κB signaling pathways, offering a potential therapeutic strategy for OA.

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