Abstract
ABSTRACT Objectives The present study was undertaken to investigate the effects and related mechanisms of hypothermia on oxidative stress and apoptosis caused by cardiac arrest (CA)-induced brain damage in rats. Methods The CA/CPR model was initiated by asphyxia. Body temperature in the normothermia and hypothermia groups was maintained at 37°C ± 0.2°C and 34°C ± 0.2°C, respectively, by surface cooling with an ice pack. First, neurological deficit scores (NDSs) were assessed, and then hippocampus samples were collected at 24 and 72 h after return of spontaneous circulation (ROSC). Results The NDSs of rats were significantly reduced after CA, and hypothermia ameliorated neurological deficits. Varying degrees of changes in cellular nuclei and mitochondria were observed in the hippocampus following CA; however, morphological changes became less apparent after therapeutic hypothermia. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were higher in the hippocampus at 24 h after ROSC. In contrast, hypothermia did not alter MDA content, while SOD activity further increased. Furthermore, hypothermia reversed the caspase-3 enhancement observed in the normothermia group at 24 h after ROSC. CA also inhibited GSK-3β phosphorylation, promoted Nrf2 translocation to the nucleus, and downregulated HO-1 expression. However, hypothermia significantly reversed these CA-induced changes in GSK-3β phosphorylation, Nrf2 translocation, and HO-1 expression. Conclusion Hypothermia attenuated CA-induced neurological deficits and hippocampal morphology changes in rats. The protective effect of hypothermia following CA may have been related to inhibition of oxidative stress and apoptosis, and its underlying mechanisms may have been due, at least in part, to activation of the GSK-3β/Nrf2/HO-1 pathway.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call