Neuroprotective effects of gap junction blocker octanol on cerebral ischemia-reperfusion injury in rats may be associated with the alleviation of inflammatory response / 国际脑血管病杂志

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-1 [β,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.