This work investigates the effects of oxidative stress due to exhaustive training on uncoupling protein 2 (UCP2) and Bcl-2/Bax in rat skeletal muscles. A total of 18 Sprague-Dawley female rats were randomly divided into three groups: the control group (CON), the trained control group (TC), and the exhaustive trained group (ET). Malondialdehyde (MDA), superoxide dismutase (SOD), xanthine oxidase (XOD), ATPase, UCP2, and Bcl-2/Bax ratio in red gastrocnemius muscles were measured. Exhaustive training induced ROS increase in red gastrocnemius muscles, which led to a decrease in the cell antiapoptotic ability (Bcl-2/Bax ratio). An increase in UCP2 expression can reduce ROS production and affect mitochondrial energy production. Thus, oxidative stress plays a significant role in overtraining.

Interleukin (IL)‐27 is a new member of the IL‐6/IL‐12 family, composed of two subunits, the Epstein–Barr virus–induced gene 3 (EBI3) and p28 chains (p28), and produced by activated monocytes and dendritic cells. IL‐27 plays an important role in the regulation of differentiation of naive T helper cells and has diverse effects on innate immune cells. However, the pro‐inflammatory mechanisms of IL‐27 are still not well known. In this study, we investigated the effect of lipopolysaccharide (LPS) on the production of IL‐27. We found that LPS‐stimulated IL‐27 production was in a dose‐dependent and time‐dependent manner in THP‐1 cells. We have also shown that IL‐27 induced PGE2 production and COX‐2 gene expression at the level of mRNA as well as protein. Moreover, we found feed back effect of PGE2 on the production of IL‐27 in THP‐1 cells. The results suggest that PGE2 significantly inhibits LPS‐induced IL‐27 production, without affecting basal IL‐27 expression. Further experiment suggests that PGE2 and LPS regulate IL‐27 through NF‐κB pathway. Our findings may have wide implication for IL‐27 in inflammatory diseases.