Akt, a key protein of cell survival, can promote cell growth and survival by activations of various cellular protective factors. Ischemic preconditioning (IP) has been known to reduce ischemic injury through upregulation of phosphorylation of Akt (p-Akt). CuZn-superoxide dismutase (SOD-1), an antioxidant enzyme, scavenges reactive oxygen species and protects cell from oxidative stress by increasing the activaiton of Akt.
The present study was performed to examine the effects of IP on the expression of p-Akt and SOD-1 in the ischemicreperfused rat skeletal muscles.
Thirty weeks old male SD rats were divided into 4 groups, such as controls, IP, 4 hour ischemia and 4 hour ischemia with IP. For IP, commom iliac artery was occluded three times for 5 min ischemia followed by 5 min reperfusion using rodent vascular clamps. Ischemia was induced by occlusion on the same artery for 4 hours. The Tibialis anterior and Soleus were removed at 0, 1, 3, and 24 hours of reperfusion. The expressions of p-Akt (Ser 473) and SOD-1 were examined with immunohistochemistry and Western blot analysis.
In the IP group, the p-Akt and SOD-1 were increased, compared to the control group. In the ischemia group, the p-Akt and SOD-1 were decreased, compared to the control group, and were more abundant when reperfusion time were increased. IP increased the p-Akt and SOD-1 after 4 hour ischemia, and the p-Akt and SOD-1 were higher in Soleus compared to Tibialis anterior.
These findings suggest that IP increases p-Akt and expression of SOD-1 in the ischemic-reperfused rat skeletal muscles, and that upregulations of p-Akt and SOD-1 induced by IP were higher in the red muscle fiber, Soleus, than the white muscle fiber, Tibialis anterior.