Protective Effect Of Ligustrazine On Glutamate Induced Neurotoxicity In The Hippocampal Neurons

The hippocampus is critical for the formation of new autobiographical and fact memories. It may be function as a memory "gateway" through which new memories must pass before entering permanent storage in the brain. Hippocampal damage can result in anterograde amnesia: loss of ability to form new memories, although older memories may be safe. The hippocampus is especially sensitive to global reductions in oxygen level in the body. The hippocampus is also a common focus site in epilepsy, and can be damaged through chronic seizures. It is also sometimes damaged in diseases such as herpes encephalitis, and is one of the first brain areas to show damage in Alzheimer's disease. Glutamate is a powerful excitatory neurotransmitter which it is released by nerve cells in the brain. In many cases, cells activated by glutamate become overexcited. This overexcitation can lead to effects that can cause cell damage and/or death. The damage of glutamic overexcitation is a common course of many diseases such as cerebral ischemia, AD, HD, et al. The traditional medicine, Chinese herb is one of the most effective methods to treat the central nerve system disease, and the herb of Ligustrazine may be beneficial to the injury of neurons induced by the exitotoxicity of glutamate which is one of the key role in many disease courses.Objective To observe the protective effect of ligustrazine on glutamate-induced injury in culture hippocampal neurons.Methods Primarily cultured hippocampal neurons from newly born rat were incubated with Ligustrazine (10μmol/L) for 12 hours, then glutamate (1mmol/L) was added for 20 minutes to induce injury. Cell viability was detected by MTT assay, and the vigor of LDH was determined by biochemistry method. In the end, the protein of AchE in the cultured neurons was performed according to the protocol of immuocytochemistry.Results After the pretreatment with the ligustrazine for 12 hours, the survival rate of cultured hippocampal neurons was increased 28.78% compared to the normal group(P<0.01), and the most suitable concentration of Ligustrazine is 10μmol/L. The neural processes were shorten and the refragibility of cultured cells desecened when neurons were injuryed by 1mmol/L glutamate. When the injury neurons induced by glutamate were treated by Ligustrazine the morphous of those cells were improved, survival rate of neurons was increased(P<0.01), and the ratio of LDH leakage from the injury kytoplasm was decreased(P<0.01). The expression of the AchE in the injury neurons was promoted by the pretreatment of the Ligustrazine.Conclusion (1) Ligustrazine could significantly increase the survival rate of primary cultured hippocampal neuron and improve its growth. The most effective concentration is 10μmol/L. (2)The exitotoxicity of glutamate could be diluted by Ligustrazine, and the possible mechanism of the protective effection might involve in improving the stability and integrity of cytomembrane and obstructing the injury by glutamte. (3) Ligustrazine could inhibit the neural functional damage, improve the expression of protein AchE and decrease the neural death when the neural cells induced the injury with the glutamate.