การพัฒนาวิธีการรักษาการบาดเจ็บของเส้นประสาทโดยการเปลี่ยนแปลงระดับการกระตุ้นของ MAPKs : รายงานการวิจัย / สิทธิพร แอกทอง = Development of treatment for nerve injury by modulating the activation of MAPKs / Sithiporn Agthong
Nerve injury remains the major cause of disability due to neuronal and glial cell apoptosis. Evidence suggests the possible role of p38 in these events. This study was aimed to examine the status of p38 in spinal ganglia and sciatic nerve after injury and to test if p38 is involved in the apoptosis. Complete injury (transection) of sciatic nerve was induced in rats and the tissues were removed for determining the levels of p38 and apoptosis-related proteins after 2 weeks. In another experiment, the rats received either specific p38 inhibitor (SB203580) 200 g/kg/day i.p. (inhibitor group) or vehicle (DMSO) only (control group) and the tissues removed at 2 weeks post-injury. Western blot showed no changes in the ratio of active to total p38 (p38-P/T) which indicates its status, in the DRG and sciatic nerve after injury. Results of the p38 substrate, ATF2, were similar. However, the expression of total caspase-3 was increased after injury. Immunohistochemistry showed the main locations of these proteins in the DRG neurons and Schwann cells. With the p38 inhibitor, activities of p38 and ATF2 including levels of total caspase-3 were decreased, especially in the DRG. These data indicates that p38 is likely involved in the apoptosis of DRG neurons after nerve injury which should be verified by direct studies on the apoptosis.
