抄録
Regular exercise protects against harmful consequences of reactive oxygen species (ROS) and represents an effective and cost-efficient strategy for the prevention of a wide variety of diseases, which are often caused by oxidative stress. ROS generated during inflammation can lead to an increase in cell proliferation, survival, and inhibition of pro-apoptotic pathway, ultimately resulting in carcinogenesis. Exercise has been considered to reduce colon carcinogenesis by potentiating cellular defense mechanisms that protect against detrimental effects mediated by ROS. The present study was aimed to examine a possible protective effect of regular exercise against oxidative stress and inflammation induced by dextran sulfate sodium (DSS) in mouse colon. Administration of 3% DSS in drinking water to male ICR mice for 7 days resulted in a decreased body weight, bloody stool, diarrhea and a shortened colon length. The expression of COX-2 and iNOS, two representative pro-inflammatory enzymes, was elevated. The expression of COX-2 and iNOS is regulated by NF-κB. Short-term treadmill running exercise prior to administration of 3% DSS attenuated colitis and reduced the expression of COX-2 and iNOS by blocking NF-κB signaling, while the levels of glutathione, the principal cellular non-enzymatic antioxidant, were increased. Long-term exercise further decreased the expression of inflammatory factors and elevated GSH levels. In conclusion, regular exercise protected against DSS-induced inflammation and ROS-mediated oxidative stress in mouse colon by targeting NF-κB pathways, suggesting potential for prevention of inflammation-associated colon carcinogenesis.
