How
hypothermia serves an early protective role against
cerebral ischemia remains to be determined. The small ubiquitin‑related modifier
protein (SUMO) functions as a post‑translational modification system and SUMO‑2/3 subtypes are often activated in early stress. The present study investigated changes in the
protein level of SUMO using western blotting and immunocytochemistry when neurons were exposed to oxygen‑glucose deprivation (OGD) in vitro, as well as in a rat model of
middle cerebral artery occlusion (MCAO) in vivo. The results demonstrated that a large number of
proteins were conjugated to SUMO‑2/3 in OGD‑injured neurons (within 10 min, peaking at 12 h), and was markedly enhanced under conditions of
hypothermia (33˚C). Concordantly,
lactate dehydrogenase (LDH) release and the apoptosis rate, as determined by LDH and TUNEL assays, respectively, were lower in hypothermia‑treated neurons. Similar results were obtained in a rat model of MCAO. Neurological deficit scores were lower in the
hypothermia group than in the
sham group in the early stage of
cerebral ischemia (P<0.05). However, no significant differences in neurological deficit scores were detected between the
hypothermia group and the
sham group in the late stage of
ischemia (21 days; P>0.05). This study implicates a role for SUMO‑2/3 in early hypothermia‑induced neuroprotection against
stroke. The development of small molecule
therapeutics based on SUMO‑2/3 may benefit patients with
cerebral ischemia.