Preventive effect of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) against endotoxin-induced muscle atrophy.

BACKGROUND & AIMS:Muscle atrophy is a public health issue and inflammation is a major cause of muscle atrophy. While docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), which are typical ω-3 polyunsaturated fatty acids, are reported to have anti-inflammatory effects on endotoxin-induced inflammatory responses, their effects on inflammatory muscle atrophy have not been clarified. In this study, we aimed to investigate the effects of DHA and EPA on inflammatory muscle atrophy. METHODS:DHA or EPA was added to C2C12 myotubes at a concentration of 25, 50, or 100 μM, and 1 h later, lipopolysaccharide (LPS) was added at a concentration of 1 μg/mL. Two hours after the first LPS addition, mRNA expression of atrogin-1 and Murf-1 in C2C12 myotubes was measured. The second LPS addition was performed 24 h after the first LPS addition, and myotube diameter, myofibrillar protein, and cell viability were measured. One-way ANOVA and Tukey's multiple comparison test were used for statistical processing of the results, and the significance level was set to less than 5 %. RESULTS:The LPS-added group significantly decreased the myotube diameter and the myofibrillar protein content compared to the control group. The myotube diameter was significantly higher in the 25 μM, 50 μM DHA and 25 μM EPA-added groups compared to the LPS group. In the 25 μM DHA and EPA-added groups, the myofibrillar protein content was significantly higher than that in the LPS group. The mRNA expression levels of atrogin-1 and murf-1 were significantly suppressed in the 25 μM DHA and EPA-added groups compared to the LPS group. The cell viability did not change by the addition of LPS, DHA, and EPA. CONCLUSIONS:The addition of DHA or EPA suppressed the decrease in myotube diameter and myofibrillar protein content and suppressed the increase in atrogin-1 and murf-1 induced by LPS. This study showed the preventive effect of DHA and EPA on endotoxin-induced muscle atrophy.