Capsaicin protects against atrophy in human skeletal muscle cells

Abstract

Skeletal muscle atrophy occurs in many pathological conditions, e.g. AIDS, cancer, sepsis and starvation, and with increased age. There is currently no effective treatment to prevent or reverse this muscle wasting. The TRPV1 agonist, capsaicin, has previously been shown to have a protective effect against skeletal muscle atrophy in mice as well as stimulate hypertrophy. We therefore investigated the effects of capsaicin against dexamethasone-induced atrophy in human primary skeletal muscle myotubes. By treating myotubes with 50μM dexamethasone we successfully induced atrophy, and saw a significant decrease in total protein content as well as MYH2 expression without a change in the atrophy genes BNIP3, GABARAPL1 and FBXO32. 100nM capsaicin treatment in isolation had no effect on protein content but significantly elevated the expression of MYH2 and MYOG above that of dexamethasone-treated cells as well as untreated control. However when combined with dexamethasone, capsaicin reduced some of the negative effects seen previously with dexamethasone alone. The addition of TNFα to the cell culture medium failed to induce atrophy in these myotubes. From the findings of this initial experiment it can be conclude that capsaicin has the capacity to protect against dexamethasone-induced atrophy in these human skeletal myotubes.