Journal of oral & facial pain and headache · 2025
Loss of SCRG1 in chondrocytes inhibits osteoarthritis by promoting autophagy activity in the temporomandibular joint through inhibition of neurokine receptors.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Zhang JiaJun, Yuan LePing, Zhang YanYan, Jin HaoYang, Zhao YeKe, Zeng XiaoKe, Zou YanHui, Wang KeYu, Nie Xin
Аннотация
BACKGROUND: To investigate in vitro how scrapie responsive gene 1 (SCRG1) contributes to the development of temporomandibular joint osteoarthritis (TMJOA).
METHODS: Western blotting was used to identify protein expression. Proinflammatory cytokine levels were assessed by means of an enzyme-linked immunosorbent test. In order to find out whether chondrocytes expressed protein light chain 3B (LC3B), immunofluorescence was utilized.
RESULTS: In the TMJOA in vitro model, hydrogen peroxide (H2O2) treatment increased the expression of SCRG1, stimulated chondrocyte catabolism and inflammatory response, and blocked autophagy. In chondrocytes, SCRG1 silencing reduces the inflammatory response, catabolism, and autophagy inhibition brought on by H2O2. Concurrently, H2O2 induction triggers the nuclear factor (NF)-κB pathway and nerve growth factor receptor (NGFR). When SCRG1 is downregulated, NGFR expression is inhibited and the NF-κB pathway is blocked.
CONCLUSIONS: By inhibiting NGFR and blocking the NF-κB pathway, knocking down SCRG1 can prevent H2O2-induced inflammatory response, metabolic breakdown and autophagy inhibition in chondrocytes.
METHODS: Western blotting was used to identify protein expression. Proinflammatory cytokine levels were assessed by means of an enzyme-linked immunosorbent test. In order to find out whether chondrocytes expressed protein light chain 3B (LC3B), immunofluorescence was utilized.
RESULTS: In the TMJOA in vitro model, hydrogen peroxide (H2O2) treatment increased the expression of SCRG1, stimulated chondrocyte catabolism and inflammatory response, and blocked autophagy. In chondrocytes, SCRG1 silencing reduces the inflammatory response, catabolism, and autophagy inhibition brought on by H2O2. Concurrently, H2O2 induction triggers the nuclear factor (NF)-κB pathway and nerve growth factor receptor (NGFR). When SCRG1 is downregulated, NGFR expression is inhibited and the NF-κB pathway is blocked.
CONCLUSIONS: By inhibiting NGFR and blocking the NF-κB pathway, knocking down SCRG1 can prevent H2O2-induced inflammatory response, metabolic breakdown and autophagy inhibition in chondrocytes.