Oral diseases · 2025
Trehalose Alleviates the Advancement of Temporomandibular Joint Osteoarthritis via Regulating the AMPK/ULK1 Autophagy Pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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Xu Jingjing, Liu Yanjiao, Zhu Siqi, Yu Wanping, Kang Hong, Bao Guangjie
Аннотация
OBJECTIVE: TMJOA is a chronic degenerative joint disorder with multiple etiologies that significantly impair patients' quality of life. Autophagy and apoptosis are critical to the pathogenesis of TMJOA. Trehalose is a novel autophagy activator and has significant therapeutic efficacy in mitigating diseases. This study investigated trehalose's role and possible mechanisms in TMJOA evolution, both in vitro and in vivo.
METHODS: Rat condylar chondrocytes were identified by toluidine blue and type I/II collagen immunofluorescence staining. Methods such as CCK-8 assay and immunofluorescence were used to detect the protective effect of trehalose on interleukin-1β (IL-1β)-induced chondrocytes. Histological staining and other techniques were applied to evaluate its therapeutic effect on monosodium iodoacetate (MIA)-induced TMJOA in rats and its underlying mechanism.
RESULTS: Trehalose can suppress IL-1β-induced apoptosis in condylar chondrocytes by stimulating autophagy through the activation of AMP-activated kinase (AMPK) and UNC51-like kinase-1 (ULK1). The inhibition of the AMPK signaling pathway negated the preventive effect of trehalose on TMJOA. TMJOA rats treated with trehalose exhibited phosphorylation of the AMPK/ULK1 pathway and activation of autophagy, accompanied by cartilage protection.
CONCLUSIONS: This study demonstrates the potential of trehalose as a novel treatment agent to impede the evolution of TMJOA.
METHODS: Rat condylar chondrocytes were identified by toluidine blue and type I/II collagen immunofluorescence staining. Methods such as CCK-8 assay and immunofluorescence were used to detect the protective effect of trehalose on interleukin-1β (IL-1β)-induced chondrocytes. Histological staining and other techniques were applied to evaluate its therapeutic effect on monosodium iodoacetate (MIA)-induced TMJOA in rats and its underlying mechanism.
RESULTS: Trehalose can suppress IL-1β-induced apoptosis in condylar chondrocytes by stimulating autophagy through the activation of AMP-activated kinase (AMPK) and UNC51-like kinase-1 (ULK1). The inhibition of the AMPK signaling pathway negated the preventive effect of trehalose on TMJOA. TMJOA rats treated with trehalose exhibited phosphorylation of the AMPK/ULK1 pathway and activation of autophagy, accompanied by cartilage protection.
CONCLUSIONS: This study demonstrates the potential of trehalose as a novel treatment agent to impede the evolution of TMJOA.