Gp91ds-tat attenuates neuronal damage in hippocampal CA1 region induced by ischemia/reperfusion through inhibiting the JNK3/c-Jun signaling pathway

Objective To investigate whether the protective effects of NOX2 inhibitor Gp91ds-tat on neuronal ischemia/reperfusion damage in rat hippocampal CA1 region are associated with inhibition of the JNK3/c-Jun signaling pathway. MethodsA brain ischemia model of rats was established using the four-vessel occlusion methods. SD rats were randomly divided into a sham group, an ischemia/reperfusion (I/R) group, a normal saline group and a Gp91-tat (Gp) group. The normal saline and Gp groups were injected with normal saline and 0.4 μg /kg Gp91ds-tat into the lateral ventricle 20 min before global cerebral ischemia. The levels of JNK3, P-JNK3, c-Jun and P-c-Jun in hippocampal CA1 region of rats were detected by immunoblotting. The survival of neurons was observed in hippocampal CA1 region. ResultsOn Day 1 of I/R, compared with the I/R group, the Gp group showed remarkable decreases in the levels of phosphorylated JNK3 and c-Jun (P<0.05). Meanwhile, the number of viable neurons were higher in the Gp group than those in the I/R group (P<0.05). ConclusionsGp91ds-tat has protective effects on the I/R damage of hippocampal CA1 neurons in rats, which may be achieved through inhibiting the JNK3/c-Jun signaling pathway.