氟桂利嗪对体外培养海马神经元缺血缺氧损伤的影响及其机制的初步研究

目的　利用氟桂利嗪 (FNZ)研究钙离子拮抗剂对体外培养海马神经元缺血缺氧损伤的作用及其作用机制。方法　利用体外培养的海马神经元 ,通过去除培养液中的糖和氧气来模拟脑缺血缺氧 ,观察不同浓度FNZ对缺血缺氧海马神经元的形态学、乳酸脱氢酶 (LDH)和细胞存活率的影响 ,并观察FNZ对Bcl 2、BDNF蛋白表达的影响。结果　在一定浓度范围之内 ,FNZ可对缺血缺氧神经元起到保护作用 ,过高浓度不但没有保护作用 ,反而加重损伤。缺血缺氧可使Bcl 2蛋白表达明显下降 ,BDNF蛋白表达明显上升 ,FNZ(5 0 μmol/L)可使缺血缺氧神经元Bcl 2表达明显升高 ,BDNF表达下降。结论　在一定浓度范围之内FNZ可保护缺血缺氧神经元 ,可能与诱导Bcl 2蛋白表达和抑制BDNF蛋白表达有关 ;过高浓度FNZ有可能存在某种潜在毒性。

Preliminary study of the effect of FNZ on the ischemic-hypoxic injury of hippocampal neurons cultured in vitro and its mechanism

Objective To study the dual effects of calcium antagonists on ischemic hypoxic injury of hippocampal neurons cultured in vitro by using flunarizine(FNZ) and the mechanism of its action.Methods The ischemic hypoxic model was established by combined deprivation of glucose and oxygen in the medium.The morphological change,LDH and cell survival rate were examined after adding different concentrations of FNZ into the medium.The changes of Bcl 2 and BDNF protein expression were examined by immunohistochemical method.Results FNZ could not only protect the ischemic hypoxic neurons,but also increase the expression of Bcl 2 and decrease the expression of BDNF.On the contrary,it was harmful at high concentrations.Conclusions FNZ has dual effects in vitro.It may have some kind of harmful effect at high concentrations.