Effect of gap junction blocker octanol on mitogen activated protein kinase signal pathway after cerebral ischemia reperfusion in rats

Abstract

Objective To investigate the effect of octanol, a gap junction blocker, on mitogen activated protein kinase (MAPK) signal pathway after ischemia reperfusion in rats. Methods Seventy-two male SD rats were randomly divided into sham-operated group, DMSO control group, saline control group and octanol group (n=18). The focal cerebral ischemia reperfusion models were established by suture method in the later three groups. Rats were injected 5 mmol/kg octanol solution (5% octanol soluble in 5% DMSO solution) into the abdominal cavity of rats in the octanol group 30 min before ischemia reperfusion; rats in the DMSO control group were injected with same amount of 5% DMSO solution, and those in the sham-operated group and saline control group were injected with same amount of saline. At 24 h after reperfusion, Neurological Function Defect Scale was performed; water content in brain tissues was detected by dry-wet method; cerebral infarction volume percentage was detected by TTC staining; the total protein expressions of extracellular signal-regulated kinase 1/2 (ERK1/2), c-jun amino-terminal kinase (JNK), and p38, and protein expressions of phosphorylased (p)- ERK1/2, p-JNK, and p-p38 were detected by Western blotting. Results The scores of Neurological Function Defect Scale, water content in brain tissues, and infarction volume percentage of the octanol group (1.583±0.651, 78.363%±0.672%, and 24.34%±0.19%) were obviously reduced as compared with those in the DMSO control group (2.344±0.743, 80.873%±0.831%, and 32.26%±0.21%) and saline control group (2.351±0.732, 80.893%±0.734%, and 32.28%±0.24%), with significant differences (P<0.05). The protein expressions of p-ERK1/2, p-JNK, and p-p38 in the octanol group (0.201±0.009, 0.211±0.011, and 0.191±0.009) were obviously reduced as compared with those in the DMSO control group (0.389±0.019, 0.311±0.022, and 0.309±0.021) and saline control group (0.393±0.021, 0.304±0.021, and 0.316±0.025), with significant differences (P<0.05). Conclusion Octanol can reduce ischemic reperfusion injury, whose mechanism may be related to the regulation of MAPK signal pathway. Key words: Cerebral ischemia reperfusion; Octanol; Gap junction; Mitogen activated protein kinase