Near-infrared light-triggered polypyrrole promotes C2C12 cell differentiation and inhibits TNF-α induced myotube atrophy

Cell Signal. 2022 Dec:100:110463. doi: 10.1016/j.cellsig.2022.110463. Epub 2022 Sep 6.

Abstract

Treatment of skeletal muscle atrophy and strengthening the muscles remain a challenge in modern medicine. Studies have shown that photobiomodulation can inhibit skeletal muscle atrophy and aid in functional recovery. Near-infrared radiation (NIR) therapy has emerged as a complementary therapy for the treatment of skeletal muscle atrophy, but its underlying mechanism remains unclear. Polypyrrole (PPy) is an organic polymer with strong near-infrared absorption, which can generate heat from absorbed NIR. In this study, MHC immunofluorescence staining was performed on C2C12 myoblasts to investigate the differentiation of C2C12 cells after NIR-triggered PPy exposure. As TNF-α-induced C2C12 myotubes were used as a model of muscular atrophy. Giemsa staining was used to determine the myotube diameter. Western blot analysis was performed to examine the proteins involved in the differentiation and atrophy of muscle cells, as well as in the Akt/P70S6K signaling pathway. PPy triggered by NIR promoted the differentiation of C2C12 cells, inhibited C2C12 myotube atrophy caused by TNF-α, and downregulated the expression levels of Atrogin-1 and MuRF 1 protein. In addition, we determined that Akt/P70S6K signaling pathway activity plays a crucial role in the therapeutic effect of NIR-triggered polypyrrole, which was further confirmed by the administration of the Akt inhibitor GDC0068. The optimal conditions for these effects were a PPy concentration of 0.125 mg/ml and NIR exposure for 80 s. We show that the photothermal effect of PPy triggered by near-infrared light can increase the beneficial effects of NIR, promote the differentiation of C2C12 cells, and improve C2C12 myotube atrophy, laying a foundation for its future clinical use.

Keywords: Atrophy; C2C12; Differentiation; Near-infrared radiation; Polypyrrole.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Differentiation
  • Cell Line
  • Humans
  • Muscle Fibers, Skeletal / metabolism
  • Muscle, Skeletal / metabolism
  • Muscular Atrophy / metabolism
  • Polymers* / metabolism
  • Polymers* / pharmacology
  • Polymers* / therapeutic use
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pyrroles / pharmacology
  • Ribosomal Protein S6 Kinases, 70-kDa / metabolism
  • Tumor Necrosis Factor-alpha* / metabolism
  • Tumor Necrosis Factor-alpha* / pharmacology

Substances

  • polypyrrole
  • Polymers
  • Tumor Necrosis Factor-alpha
  • Pyrroles
  • Ribosomal Protein S6 Kinases, 70-kDa
  • Proto-Oncogene Proteins c-akt