Lutein Modulates Chondrocyte Autophagy In Tmj Ankylosis Via Pi3k/Akt

To investigate the mechanism of lutein-mediated autophagy regulation in traumatic temporomandibular joint ankylosis (TMJA) chondrocytes through the PI3K/AKT pathway. Thirty-two male New Zealand rabbits were randomized into four groups (n=8): Sham, Model, Lutein (10 mg/kg), and Lutein+3-MA (15 mg/kg). TMJA models were established through surgical induction, with drug interventions initiated 24 h post-operation via weekly tail vein injections for 12 weeks. Cartilage tissues were analyzed using histopathology, Western blot (PI3K, p-AKT, LC3-II, Beclin-1, Aggrecan, Collagen II), and immunofluorescence. The Model group exhibited significantly elevated pathological scores versus Sham (4.32±0.51 vs 1.05±0.23, *P*<0.05). Molecular analysis revealed decreased PI3K phosphorylation (0.38±0.07 vs 1.00±0.00) and p-AKT expression (0.42±0.09 vs 1.00±0.00), accompanied by upregulated autophagy markers (LC3-II: 2.15±0.31; Beclin-1: 1.87±0.28) and extracellular matrix degradation (Aggrecan: 0.41±0.06; Collagen II: 0.39±0.05). Lutein treatment significantly reversed these abnormalities (*P*<0.05 vs Model). Conversely, 3-MA coadministration abolished lutein's therapeutic effects. Lutein exerts chondroprotective effects in TMJA by restoring PI3K/AKT-mediated autophagy homeostasis, providing mechanistic insights for clinical translation.