论文部分内容阅读
Recent research shows that the JNK1/2 signaling pathway plays a neuroprotective role against ischemia-reperfusion injury by cross-talk with other pathways.The present study investigated the effects of isoflurane and sevoflurane postconditioning on JNK1/2 pathway activity and neuronal cell viability after oxygen and glucose deprivation injury in hippocampal slices in vitro.Techniques used included population spike analysis,propidium iodide fluorescent staining,western blot assay,and the use of JNK1/2-specific pharmacological tools such as anisomycin (agonist) and SP600125 (inhibitor).We found that both isoflurane and sevoflurane inhibited JNK pathway activity and had neuroprotective effects against oxygen and glucose deprivation injury in slices of rat hippocampus in vitro.Postconditioning with volatile anesthetics exerted neuroprotective effects on nerve cells and preserved the function of the CA1 region by inhibiting JNK1/2 phosphorylation.This suppression of JNK1/2 activity could underlie the observed synergistic neuroprotective effect produced by volatile anesthetic postconditioning.
Recent research shows that the JNK1 / 2 signaling pathway plays a neuroprotective role against ischemia-reperfusion injury by cross-talk with other pathways. The present study investigated the effects of isoflurane and sevoflurane postconditioning on JNK1 / 2 pathway activity and neuronal cell viability after oxygen and glucose deprivation injury in hippocampal slices in vitro. Techniques used included population spike analysis, propidium iodide fluorescent staining, western blot assay, and the use of JNK1 / 2-specific pharmacological tools such as anisomycin (agonist) and SP600125 (inhibitor) found that both isoflurane and sevoflurane inhibited JNK pathway activity and had neuroprotective effects against oxygen and glucose deprivation injury in slices of rat hippocampus in vitro. Postconditioning with volatile anesthetics exerted neuroprotective effects on nerve cells and preserved the function of the CA1 region by inhibiting JNK1 / 2 phosphorylation.This suppression of JNK1 / 2 activity could und erlie the observed synergistic neuroprotective effect produced by volatile anesthetic postconditioning.