Skeletal muscle atrophy is closely associated with oxidative stress-induced inflammatory responses,which lead to the activation of catabolic pathways and the loss of myotube integrity. Dillapiole, a phenylpropanoid compound derived from several aromatic plants, has been reported to exhibit anti-inflammatory and antioxidant properties, suggesting its potential benefits in conditions characterized by muscle wasting. This study aimed to investigate whether dillapiole attenuates hydrogen peroxide (H2O2 )-induced muscle atrophy in C2C12 myotubes and to elucidate its regulatory effects on key atrogenes. C2C12 myoblasts were differentiated into myotubes and then exposed to H2O2 to induce oxidative stress-mediated atrophy in the presence or absence of dillapiole. These findings indicate that dillapiole protects C2C12 myotubes against H2O2-induced muscle atrophy primarily by attenuating oxidative stress–associated inflammatory responses and suppressing the expression of Atrogin-1 and MuRF1.

Reserpine is a well-known medicine for the treatment of hypertension, however the role of reserpine in cell signaling is not fully understood. Here, we report that reserpine treatment induces the phosphorylation of AMP activated protein kinase (AMPK) at threonine 172 (T172) in PC12 cells. Phosphorylation of AMPK T172 is regulated by upstream signaling molecules, and the increase of phospho-T172 indicates that AMPK is activated. When we examined the FOXO3a dependent transcription by using the FHRE-Luc reporter assay, reserpine treatment repressed the FHRE-Luc reporter activity in a dose dependent manner. Finally, we showed that reserpine treatment induced the phosphorylation of AMPK as well as cell death in MCF-7 cells. These results suggest that AMPK is a potential cellular target of reserpine.
AMP-Activated Protein Kinases* ; Animals ; Cell Death ; Hypertension ; MCF-7 Cells ; PC12 Cells ; Phosphorylation ; Reserpine* ; Threonine