Procaine at Low Concentration Modulates Mitochondrial Features in Cultured Fibroblasts and Myoblasts: A Clue to the Cellular Mechanisms Underlying Neural Therapy.

Abstract

Procaine is a local anesthetic used at low concentrations in a complementary medical approach, neural therapy, due to its ability to promote antioxidant and anti-inflammatory response. Previous biochemical studies showed that low concentrations of procaine may also stimulate mitochondrial function. In the present study, low procaine concentrations were used to investigate in vitro the effects on mitochondria of human fibroblasts and mouse myoblasts. Histochemical, ultrastructural, and biomolecular techniques were employed. After 24 h from procaine treatment, mitochondrial membrane potential was unaltered in both cell types, but some mitochondrial features showed cell-specific modifications. In detail, in fibroblasts, procaine induced decreased mitochondrial cristae length and cellular adenosine triphosphate (ATP) levels. In myoblasts, procaine induced modifications of mitochondrial shape and oxidative phosphorylation subunit amount, together with increased cellular ATP levels. Most modifications were restored at 48 h. To explain the differential response of the two cell lines, we hypothesize a species-specific sensitivity to procaine or a cell-specific sensitivity related to the different extent of the endoplasmic reticulum, which is especially susceptible to procaine. Taken together, the results of this pilot study show that procaine at low concentration exerts a modulatory effect on mitochondrial features, opening the way to further studies aimed at elucidating the cellular pathways involved in the beneficial effects observed in procaine-based neural therapy.