Liproxstatin-1 alleviates cartilage degradation by inhibiting chondrocyte ferroptosis in the temporomandibular joint.
Biol Cell
; 116(1): e202300042, 2024 Jan.
Article
em En
| MEDLINE
| ID: mdl-37919852
ABSTRACT
BGROUND INFORMATION Ferroptosis contributes to temporomandibular joint osteoarthritis (TMJOA) lesion development and is still poorly understood. RESULTS:
In this study, we used different TMJOA animal models to examine whether ferroptosis was related to disease onset in TMJOA induced by monosodium iodoacetate (MIA), IL-1ß, occlusion disorder (OD), and unilateral anterior crossbite (UAC). Immunohistochemical staining and Western blot analysis were used to detect ferroptosis- and cartilage degradation-related protein expression. Our results revealed reduced levels of the ferroptosis-related protein GPX4 in the cartilage layer, but the levels of ACSL4 and P53 were increased in the condyle. Injection of the ferroptosis inhibitor liproxstatin-1 (Lip-1) effectively decreased ACSL4, P53 and TRF expression. In vitro, IL-1ß reduced cartilage extracellular matrix expression in mandibular condylar chondrocytes (MCCs). Lip-1 maintained the morphology and function of mitochondria and ameliorated the exacerbation of lipid peroxidation and reactive oxygen species (ROS) production induced by IL-1ß.CONCLUSION:
These results suggest that chondrocyte ferroptosis plays an important role in the development and progression of TMJOA.SIGNIFICANCE:
Inhibiting condylar chondrocyte ferroptosis could be a promising therapeutic strategy for TMJOA.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Quinoxalinas
/
Compostos de Espiro
/
Cartilagem Articular
/
Ferroptose
Limite:
Animals
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article