Effect of Taraxasterol on Akt1-Dependent Inflammatory and Myogenic Pathways in Human Skeletal Muscle Cells Under Lipopolysaccharide-Induced Inflammation

Abstract

Introduction: This study aimed to investigate the effects of Taraxasterol on proliferation and inflammatory and myogenic pathways related to Akt1 signaling in human skeletal muscle cells, using an in vitro model of lipopolysaccharide-induced inflammation.

Methods: Human skeletal muscle cell line (C436) was cultured in vitro in basal medium or medium containing lipopolysaccharide (concentration 0.1 μg/ml) and/or taraxasterol (concentrations 5, 10, and 15 μM). After 24 hours, the MTT test was used to measure cell proliferation. Then, the optimal concentration of taraxasterol and treatment time were selected. Real-time PCR analysis was used to detect the levels of inflammatory factors, myogenic factor, and Akt1 expression. Results: Taraxasterol significantly increased cell proliferation at concentrations of 5, 10, and 15 μg/mL after 24 hours by 1.05, 1.07, and 1.05-fold (P≤0.05). Lipopolysaccharide significantly increased the expression of TNF-α, IL-1β, and IL-6 genes by 4.32, 3.35, and 3.99-fold (P≤0.05), while taraxasterol significantly decreased the expression of each gene at all three concentrations compared to the lipopolysaccharide group (P≤0.05). Lipopolysaccharide significantly reduced the expression of Akt1, myogenin, and MyoD1 genes by 15, 68, and 65% (P≤0.05), while taraxasterol significantly increased the expression of those genes in all three concentrations compared with the lipopolysaccharide group (P≤0.05).

Conclusion: Taraxasterol can increase the proliferation of skeletal muscle cells and can also inhibit the expression of inflammatory cytokines IL-1β, IL-6, and TNF-α and enhance the expression of myogenic cytokines myogenin and MyoD1, indicating that taraxasterol may have an effect to promote cell proliferation and reduce inflammatory response in the process of relieving delayed onset muscle pain.