Effects of Sulforaphane Treatment on Skeletal Muscle from Exhaustive Exercise-Induced Inflammation and Oxidative Stress Through the Nrf2/HO-1 Signaling Pathway.

Abstract

Skeletal muscle is primarily involved in exercise performance and health promotion. Sulforaphane (SFN) is a naturally occurring isothiocyanate that indirectly activates the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), thus inducing the expression of Nrf2 target genes, including antioxidant enzymes. This study aimed to identify the effects of a single dose of SFN administration on exhaustive exercise-induced inflammation and oxidative stress in skeletal muscle tissue and elucidate the underlying mechanisms. Thirty-six mice were divided into four groups: control, SFN, exercise (Ex), and SFN + Ex. The SFN group and SFN + Ex group received SFN orally (50 mg/kg body weight) 2 h before the running test. Exercise significantly reduced plasma glucose levels, while the SFN-treated group exhibited a smaller reduction. Acute exhaustive exercise increased the expression of pro-inflammatory cytokines in muscle tissue, while the SFN + Ex group exhibited significantly reduced expression of pro-inflammatory cytokines. The gene expression of Nrf2 and its target enzymes, including heme oxygenase (HO)-1, superoxide dismutase (SOD)-1, catalase (CAT), and glutathione peroxidase (GPx)-1, was measured in the gastrocnemius and soleus muscle tissue. Compared with the Ex group, the SFN + Ex group showed upregulated expression of all these parameters, including Nrf2. SFN treatment reduced acute exhaustive exercise-induced oxidative stress and inflammation via activation of the Nrf2/HO-1 signaling pathway.