The effects of
tacrolimus postconditioning on
protein-serine-threonine kinases (Akt)
phosphorylation and apoptotic
cell death in
rats after
spinal cord ischemia -
reperfusion injury were investigated. Ninety
male SD
rats were randomly divided into sham operation group,
ischemia -
reperfusion group and
tacrolimus postconditioning group. The model of
spinal cord ischemia was established by means of
catheterization through
femoral artery and balloon
dilatation . The
spinal cord was reperfused 20 min after
ischemia via removing saline out of balloon. The corresponding
spinal cord segments were excised and determined for Akt activity in
spinal cord tissue by using
Western blotting at 5, 15, and 60 min after
reperfusion respectively.
Spinal cord tissue sections were stained immunohistochemically for
detection of the phosphorylated Akt expression at 15 min after
reperfusion .
Flow cytometry was applied to assess
apoptosis of neural
cells , and dry-wet
weights method was employed to
measure water content in
spinal cord tissue at 24 h after
reperfusion . The results showed that the activities of Akt in tarcolimus postconditioning group were significantly higher than those in
ischemia -
reperfusion group at 5, 15, and 60 min after
reperfusion (P<0.05, P<0.01). The Akt activities reached the peak at 15 min after
reperfusion in
ischemia -
reperfusion group and
tacrolimus postconditioning group. The percentage of apoptotic
cells and
water content in
spinal cord tissue were significantly reduced (P<0.01) in
tacrolimus postconditioning group as compared with those in
ischemia -
reperfusion group at 24 h after
reperfusion . It is concluded that
tacrolimus post-conditioning can increase Akt activity in
spinal cord tissue of
rats , inhibit
apoptosis of neural
cells as well as
tissue edema , and thereby alleviate
spinal cord ischemia -
reperfusion injury .