Picroside Ii Inhibits The MEK-ERK1/2 Signal Pathway To Protect The Cerebral Ischemic Injury In Rats

Objective To explore the neuroprotective effect and mechanism of picroside II on ERK1/2signal transduction pathway following cerebral ischemia injury in rats.Methods The focal cerebral ischemic models were established by inserting a monofilament threads into middle cerebral artery in 140 Wistar rats. All rats were randomly divided into control, model, picroside, LPS and U0126 groups, each group containing ischemia 6h, 12 h and 24 h subgroups. The neurobehavioral function was evaluated by modified neurological severity score points(m NSS) test. The structure of neuron was observed using hematoxylin-eosinstaining(HE) staining. The apoptotic cells were counted using terminal deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The expression of phosphorylated mitogen/extracellular signal-regulated kinase kinas1/2(p MEK1/2) and phosphorylated extracellular signal-regulated protein kinase1/2(p ERK1/2) in cortex were determined using the immunohistochemistry(IHC)and Western Blot(WB).Results The neurological behavioral malfunction appeared in all rats with MCAO. In model group, the damage of neuron was worsened, while the neurobehavioral function score, apoptotic cell index, the expression of p MEK1/2 and p ERK1/2 increased significantly compared with control group. In treatment and U0126 groups, the neurological behavioral function was improved, and the number of apoptotic cells and the expression of p MEK1/2 and p ERK1/2 decreased significantly than those in model group.In LPS group, at ischemia 6h the damage of neuron was the worst, and p MEK1/2 and p ERK1/2 expressions were much higher than those in model group. But at ischemia 12 h and 24 h the expressions of p MEK1/2 and p ERK1/2 were decreased slightly, and the neurobehavioral function was improved slightly.Conclusion Picroside II could to protect the neuron from the apoptosis and inflammation by inhibiting MEK-ERK1/2 in rats.