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

Abstract

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.