Neuroprotective effects of gap junction blocker octanol on cerebral ischemia-reperfusion injury in rats may be associated with the alleviation of inflammatory response

Abstract

Objective To investigate the effects of octanol, a gap junction blocker, on the levels of pro-inflammatory cytokines after cerebral ischemia-reperfusion in rats. Methods Seventy-two male SD rats were randomly divided into sham operation group, saline control group, vehicle group, and octanol intervention group (n=18 in each group). The model of transient middle cerebral artery occlusion was induced by the modified suture method. The octanol intervention group was intraperitoneally injected with octanol solution at 5 mmol/kg body weight 30 min before ischemia. The saline control group and the vehicle group were intraperitoneally injected with the same amount of physiological saline and 5% dimethyl sulfoxide solution 30 min before procedure. The neurological deficit score, brain water content, and cerebral infarction volume in each group were detected after ischemia for 2 h and reperfusion for 24 h. Enzyme-linked immunosorbent assay was used to detect the serum interleukin (IL) -1β, IL-6, and tumor necrosis factor-α (TNF-α) levels. Results Compared with the saline control group and the vehicle group, the neurological deficit score of the octanol intervention group was significantly lower (all P<0.05), the brain tissue water content was significantly decreased (P<0.05), the cerebral infarction volume was significantly reduced (P<0.05), and the expression levels of IL-1β, IL-6, and TNF-α were significantly decreased (all P<0.05). There were no significant differences in neurological deficit score, brain water content, cerebral infarction volume and serum IL-1β, IL-6 and TNF-α levels between the saline control group and the vehicle group. Conclusion Gap junction blocker octanol can reduce cerebral ischemic-reperfusion injury. Its mechanism may be related to the alleviation of inflammatory response. Key words: Brain ischemia; Reperfusion injury; Gap junctions; Inflammation; Cytokines; Octanols; Disease models, animal; Rats