蛋白质转导域-激肽释放酶对缺糖、缺氧后再恢复的神经元的保护作用

目的:观察蛋白质转导域-激肽释放酶(PTD-kallikrein)对缺糖、缺氧(OGD)再复糖、复氧培养的神经元保护作用,探讨其可能的作用机制。方法:以化学交联法构建PTD-kallikrein,用缓激肽B2受体抑制剂和(或)PTD-kallikrein对OGD再复糖、复氧培养的大鼠神经元进行干预,分别用MTT法及TUNEL染色测定不同条件培养的神经元生存率和凋亡。结果:PTD-kallikrein可显著提高OGD再复糖、复氧条件下培养的神经元生存率(P<0.05),并减少其凋亡(P<0.05);B2受体抑制剂能明显抑制PTD-kallikrein对神经元的保护(P<0.05)。结论:PTD-kallikrein对OGD再复糖、复氧条件下培养的神经元有明显的保护作用,并且很可能是通过B2受体的介导而发挥其功效的。

Protective Effects of PTD-kallikrein on Neurons Incubated in Condition of Oxygen-Glucose Deprivation (OGD)/Recovery

Aim:To observe the protective effects of protein transduction domain-kallikrein(PTD-kallikrein)on neurons incubated in condition of oxygen-glucose deprivation(OGD)/recovery,and to explore the protective mechanism.Methods:PTD-kallikrein was prepared by chemical synthesis.The rat neuronal cells were incubated in the condition of OGD/recovery and treated by using bradykinin B2 receptor antagonist and/or PTD-kallikrein.The neuron survival rate and apoptosis were measured by MTT and TUNEL,respectively.Results:PTD-kallikrein could dramatically increase the survival rate and decrease the apoptosis of OGD/recovery incubated neurons.However,bradykinin B2 receptor antagonist distinctly inhibits the effects of PTD-kallikrein.Conclusion:PTD-kallikrein has some neuroprotective roles to OGD/recovery incubated neurons,and its functional exertion may be involved in the mediation of bradykinin B2 receptor.