Yuki Shimizu, Keiko Hamada, Tingting Guo, Chie Hasegawa, Yusuke Kuga, Katsushi Takeda, Takashi Yagi, Hiroyuki Koyama, Hiroshi Takagi, Daisuke Aotani, Hiromi Kataoka, Tomohiro Tanaka
Biochemical and biophysical research communications 2024 Jan 29Recent studies have shown a role of inflammation in muscle atrophy and sarcopenia. However, no anti-inflammatory pharmacotherapy has been established for the treatment of sarcopenia. Here, we investigate the potential role of PPARα and its ligands on inflammatory response and PGC-1α gene expression in LPS-treated C2C12 myotubes. Knockdown of PPARα, whose expression was upregulated upon differentiation, augmented IL-6 or TNFα gene expression. Conversely, PPARα overexpression or its activation by ligands suppressed 2-h LPS-induced cytokine expression, with pemafibrate attenuating NF-κB or STAT3 phosphorylation. Of note, reduction of PGC-1α gene expression by LPS treatment for 24 hours was partially reversed by fenofibrate. Our data demonstrate a critical inhibitory role of PPARα in inflammatory response of C2C12 myotubes and suggest a future possibility of PPARα ligands as a candidate for anti-inflammatory therapy against sarcopenia. Copyright © 2023 Elsevier Inc. All rights reserved.
Yuki Shimizu, Keiko Hamada, Tingting Guo, Chie Hasegawa, Yusuke Kuga, Katsushi Takeda, Takashi Yagi, Hiroyuki Koyama, Hiroshi Takagi, Daisuke Aotani, Hiromi Kataoka, Tomohiro Tanaka. Role of PPARα in inflammatory response of C2C12 myotubes. Biochemical and biophysical research communications. 2024 Jan 29;694:149413
PMID: 38141556
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