پديد آورندگان :
Pourahmad Jalal نويسنده , REZAEI MOHSEN نويسنده , REZVANI NILOOFAR نويسنده , AHMADIANI ABOLHASSAN نويسنده
چكيده لاتين :
Programmed cell death is a highly regulated form of cell death, mostly distinguished by
the activation of a family of cystein-aspartate proteases (caspases) that cleave various proteins
resulting in morphological and biochemical changes characteristic of this form of cell death.
Several recent studies have addressed the role of programmed cell death in inflammatory and
chronic pain states. Caspase-3 plays a central role in mediating nuclear programmed cell death
including chromatin condensation and DNA fragmentation as well as cell blebbing. The aims
of this study were to investigate the effect of duration and severity of persistent pain on the
induction of programmed cell death. Formalin was administered subcutaneously in the Wistar
rat hind paws for 1,4 or 7 consecutive days, and then the activity ofcaspase-3 was measured in
both the rat liver and brain cells. Morphological changes characterizing programmed cell death
were also studied using the Sigmaיs Apoptosis Detection kit, Annexin V-Cy3. Our findings
showed that caspase-3 activity and apoptotic phenotype significantly increased in liver but not
brain cells following the increase in duration and severity of formalin induced persistent pain.