中文摘要：

碳酸锂可以用于治疗创伤和神经退行性疾病导致的脑部损伤.研究表明其保护效应与蛋白激酶C（PKC）和胞外信号调节激酶（ERK）有关.研究表明PKC激动剂PDBu可以抑制延迟整流钾通道（IK）电流并使其激活电压曲线向超极化方向移动.碳酸锂（50 μmol/L）可以抑制PDBu的反应.进一步的研究表明,预先加入MEK/ERK抑制剂U0126（20 μmol/L）,碳酸锂不能逆转PDBu对IK的作用.因此,PKC和丝裂原活化蛋白激酶（MAPK）/ERK级联反应通路可能在钾离子通道的磷酸化调节中起作用.另外,AC-cAMP和GC-cGMP的交互作用也可能参与碳酸锂对PKC激活作用的调节,成为其神经保护作用的机制之一.

英文摘要：

Lithium carbonate could be used to treat or prevent brain damage following traumatic injury and neurodegenerative diseases. It has been shown that its protective effect is related to protein kinase C （PKC） and extracellular signal-related kinase （ERK）. It was demonstrated that PDBu, a PKC activator, inhibited amplitudes of delayed rectifier potassium current （IK） and produced a hyperpolarizing shift in the activation-voltage curve. The responses to PDBu were inhibited by lithium carbonate （50μmol/L）. Further studies showed that when pretreated with MEKYERK inhibitor U0126 （20 μmol/L）, although PDBu significantly reduced IK lithium did not reverse the effect of PDBu. Thus, the results suggested that PKC signaling cascades, along with MAPK （mitogen-activated protein kinase） pathway, were required in the phosphorylation of potassium channel, which was presented by regulation of potassium channel characteristic. AC-cAMP and their cross-tall with GC-cGMP pathway could also modulate the effect of lithium on PKC activation, which could be one of underlying mechanisms likely related to neuroprotective effect of lithium.