Abstract:Objective: To investigate the nerve injury mechanism of c-Jun N-terminal kinase (JNK) in in vitro rat brain slices after oxygen glucose deprivation (OGD). Methods: The hippocampal slices of sprague dawley (SD) rats (7 days after birth) were prepared. Rats were divided into the normal control group, the model group and the inhibitor group. Brain slices in the normal group were not treated with OGD, in the model group were treated with OGD for 30 minutes, and in the inhibitor group were treated with OGD for 30 minutes and treated with 10 μmol/L SP600125.Levels of phosphorylated JNK (p-JNK) of hippocampal slices in different groups were detected by Western blot, potential changes of neurons of CA1 region in different groups were detected by whole cell patch clamp in current clamp mode, and the lactate dehydrogenase (LDH) releasing of hippocampal slices in different groups were also detected. Results: After 30 minutes of OGD, the phosphorylation level of JNK was significantly increased. Meanwhile, the potential absolute value of neurons in "resting state" was decreased, while the releasing level of LDH was increased. In addition, SP600125 was able to inhibit the phosphorylation of JNK, so as to recover the potential absolute value of neurons and inhibit the releasing of LDH (P<0.05). Conclusion: Inhibiting the over-activation of JNK signaling pathway can alleviate the neurological damage after OGD in rat hippocampal slices, and its mechanism may relate to the regulation of neuronal electrical state in "resting state" and LDH releasing.
