Chemico-biological interactions · 2026
Triphenyl phosphate may reduced oxidative muscle-fiber phenotype involving IL-17A-p38 MAPK -PGC1- α signaling pathway.
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Huang Yuting, Shi Lei, Li Yang, Ma Zhijin, Liu Keshu, Fang Shuhao, Kou Guangning
Аннотация
BACKGROUND: TPHP is widely used in various fields. In recent years, the potential health hazards of this pollutant have attracted great attention from people. However, the impact and potential mechanisms of TPHP on skeletal muscle function still need to be studied.
METHODS: This study combined in vivo animal and in vitro cell experiments. Thirty C57BL/6J mice were randomly assigned to CON, T25, and T50 groups and received 8-week TPHP gavage treatment. Gastrocnemius tissues were collected for transcriptome sequencing, qPCR, Western blotting (WB), and immunofluorescence (IF) analyses. In vitro, C2C12 myoblasts were exposed to gradient TPHP concentrations for 24 h and subjected to identical molecular detections.
RESULTS: This study showed that after intervention with TPHP, muscle atrophy markers increased in the gastrocnemius muscle of mice( p < 0.05 for T25; p < 0.01 for T50), while the expression of genes and proteins related to oxidative muscle fibers decreased( p < 0.05 for T25; p < 0.01 for T50). Gene sequencing results showed an increase in IL-17A pathway expression. Cell experiments also showed that after TPHP intervention, the expression of genes and proteins related to muscle atrophy increased in cells ( p < 0.05 for T25; p < 0.01 for T50), while the expression of genes and proteins related to oxidative muscle fibers decreased( p < 0.05 for T25; p < 0.01 for T50). By using relevant inhibitors, provides validation that the IL-17A -p38 MAPK-PGC1-α pathway can reduce oxidative muscle -fiber phenotype.
CONCLUSIONS: Our research findings indicate that TPHP may reduced oxidative muscle-fiber phenotype involving IL-17A-p38 MAPK-PGC1-α signaling pathway.
METHODS: This study combined in vivo animal and in vitro cell experiments. Thirty C57BL/6J mice were randomly assigned to CON, T25, and T50 groups and received 8-week TPHP gavage treatment. Gastrocnemius tissues were collected for transcriptome sequencing, qPCR, Western blotting (WB), and immunofluorescence (IF) analyses. In vitro, C2C12 myoblasts were exposed to gradient TPHP concentrations for 24 h and subjected to identical molecular detections.
RESULTS: This study showed that after intervention with TPHP, muscle atrophy markers increased in the gastrocnemius muscle of mice( p < 0.05 for T25; p < 0.01 for T50), while the expression of genes and proteins related to oxidative muscle fibers decreased( p < 0.05 for T25; p < 0.01 for T50). Gene sequencing results showed an increase in IL-17A pathway expression. Cell experiments also showed that after TPHP intervention, the expression of genes and proteins related to muscle atrophy increased in cells ( p < 0.05 for T25; p < 0.01 for T50), while the expression of genes and proteins related to oxidative muscle fibers decreased( p < 0.05 for T25; p < 0.01 for T50). By using relevant inhibitors, provides validation that the IL-17A -p38 MAPK-PGC1-α pathway can reduce oxidative muscle -fiber phenotype.
CONCLUSIONS: Our research findings indicate that TPHP may reduced oxidative muscle-fiber phenotype involving IL-17A-p38 MAPK-PGC1-α signaling pathway.