Effects of erythropoietin on STAT1 and STAT3 levels following cerebral ischemia-reperfusion in rats.

Background And Purpose: Cerebral ischemia-reperfusion injury can activate signal transducers and activators of transcription (STAT). STAT1 initiates neuronal apoptosis following cerebral ischemia-reperfusion, while STAT3 is neuroprotective. Erythropoietin (EPO) promotes regeneration through STAT3 and facilitates neuronal survival following ischemia. However, there are few reports on the effects of EPO on phosphorylated STAT1 (P-STAT1) level following cerebral ischemia-reperfusion in rats, and there is no evidence on the simultaneous observation of the four kinds of protein:STAT1, P-STAT1, STAT3, and P-STAT3.

Methods: We established a rat focal cerebral ischemia-reperfusion injury model, and used Western blot and immunohistochemical staining to assess the levels of STAT1 and STAT3 expression, and TdT-mediated dUTP-biotin nick end-labeling (TUNEL) was carried out to observe the number of apoptotic cells with or without EPO treatment.

Results: Our findings show that EPO treatment had no significant effect on STAT1 and STAT3 expression, but P-STAT1 and P-STAT3 were slightly decreased and significantly increased, respectively, after EPO treatment. Neurologic deficits, the infarct volume, and the number of apoptotic cells were significantly decreased after EPO treatment.

Conclusions: The results suggest that EPO exerts a neuroprotective effect by influencing STAT3 and STAT1 expression in the area injured by cerebral ischemia-reperfusion.