Investigation of the effects of intranasal Salusin-β administration on experimental cerebral ischemia/reperfusion injury in rats

Aim: The aim was to investigate the potential protective effects of intranasal Salusin-β administration in cerebral ischemia/reperfusion(I/R) injury. Material and method: The Sprague Dawley male rats included in the study were divided into three groups (n=9): control, I/R, and I/R+Salusin-β. In the groups other than the control, a 90-minute ischemia was applied. One hour after ischemia, the I/R group received intraperitoneal hydroxyethyl cellulose, while the I/R+Salusin-β group was administered 300 nM Salusin-β intranasally. During the three-day reperfusion period, the rats underwent NDS, rotarod, sticky label removal, and grip strength tests. At the end of experiment animals were decapitated and brain tissues were collected. In collected brain tissues, infarct area was determined using TTC staining, and the levels of apoptosis (BCL-2) and autophagy (Beclin-1, ATG5, ATG7, and p62) proteins were analyzed using Western Blot method. Results: The NDS score and sticky label removal time of the control and I/R+Salusin-β groups were lower, while the rotarod endurance time and grip strength were higher compared to the I/R group (p<0.05). The infarct area in the I/R group was found to be larger compared to the control and I/R+Salusin-β groups(p<0.05). The levels of BCL-2, Beclin-1, ATG5, and ATG7 proteins were higher in the I/R+Salusin-β group compared to I/R group, while the levels of p62 proteins were lower(p<0.05). Conclusion: It was observed that Salusin-β reduced neurological deficit score. Behavioral tests showed improvement in balance-motor coordination, somatosensory functions, and strength loss. Additionally, it was found that Salusin-β reduced the infarct area caused by I/R injury. Furthermore, Salusin-β was found to inhibit apoptosis by affecting apoptotic protein levels and induce autophagy by influencing autophagic protein levels. Keywords: Apoptoz, Salusin-β, Cerebral Ischemia, Autophagy