Reactive oxygen species (ROS) are known to induced endothelial cell (EC) apoptosis and vascular smooth muscle cell (VSMC) proliferation. It has demonstrated that hyperlipidemia may impact vascular function through increased oxidative stress and synthesized ROS endogenously by inhibiting electron transport chain of mitochodria in vascular cell.
In endothelial cells, ROS may activate caspase 3 through mitochondrial pathway then lead EC apoptosis. On the other hand, ROS could produce mitogenic response through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in VSMC.
Recent study has observed that exercise training may initiate adaptations to reduce oxidative sources or up regulate antioxidative enzymes.
We subjected 4~6 month-old male Zucker rats to an 8-weeks chronic exercise training program on a motorized treadmill. A total of 12 obese rats were randomly divided into two groups, i.e sedentary group and exercise-trained group. All rats were sacrificed at 48 h after the end of their last training session to minimize acute exercise effects from the last training bout. Immunoblot analysis of harvested vessels showed that lower expression of caspase 3 and ERK1/2 in obese exercised group compared with obese standard group. However superoxide dismutase (SOD) and catalase were significantly expression in both obese and lean exercised group. The results of immunohistochemestry shown that caspase 3 and ERK1/2 were highly expression on EC and VSMC both obese sedentary group. Similarly, this phenomenon would be reversed after exercise training. It was very interesting that Cu/ZnSOD and MnSOD mRNA level has no significant change from each group. The mRNA level of glutathione peroxidase was significantly elevated but catalase mRNA level was lowered instead.
In conclusion, exercise training plays a role of vascular protection by up regulating antioxidative protein expression and decreasing caspase3 and ERK1/2 protein production in obese Zucker rat.
