Background: There Are Strong Evidences to Suggest that Nuclear Factor-Erythroid2 p45-Related Factor 2 (Nrf2) Is a Master Transcriptional Factor that Modulates a Series of Cellular
Antioxidant Enzymes, such as Superoxide Dismutase (SOD),NAD(P)H-Quinoneoxidase-1 (NQO1),Hemoxygenase-1(Ho-1), Etc. It Has Been Demonstrated that Aerobic Exercise Could Reduce Oxidative Stress in
Skeletal Muscle, but There Are Few Studies about the Role of Nrf2 Involved. In This Study, We Investigated Effects of Nrf2 in Mouse Skeletal Muscles on the Adaptation of Oxidative Stress Evoked by
Methods:Two Months Old Wild-Type Mice (C67BL/6J) and Nrf2 Knockout Mice Were Divided into Control and Exercise Groups Separately (n=8-10/Group). The Exercise Groups Were Trained on a
Treadmill for 6 Days Per Week (60 min/Day, Running at a Speed of 12m/min) for Four Weeks. Measurements of Nrf2 mRNA Expression, Nrf2-Mediated Antioxidant Proteins (SOD, NQO-1, HO-1, γ-Gutamyl Cysteine
Ligase-Catalytic (GCLC), Glutathione Peroxydase(GPX), Glutathione Reductase (GR), and Catalase (CAT)) Expressions, Reactive Oxygen Species (ROS) , Glutathione Redox Ratio (GSH/GSSG) and Maximal
Oxygen Uptake(VO2max) levels , Were Carried out after Four Weeks of Interventions.
Results: There Were No Significant Changes in ROS, GSH/GSSG and Most of the Antioxidative Proteins in Skeletal Muscles and Their VO2max in Both Nrf2 Knockout and Wild-Type Mice at the
Baseline. After Four Weeks of Aerobic Exercise Training, Nrf2 Knockout Mice Presented Significant Lower ROS, GSH/GSSG, the Expressions of Antioxidative Proteins(CAT, NQO1-1, GCLC, HO-1, SOD2) and
VO2max than Those of the Wild-Type Mice.
Conclusions: It Was Suggested that Aerobic Exercise Training Could Reduce Oxidative Stress via the Nrf2- Mediated Antioxidant Actions in Mouse Skeletal Muscle.