囊泡单胺类转运体功能抑制对PC12细胞的毒性及抗氧化剂的干预

Function inhibition of vesicular monoamine transporter on intervention of toxicity and antioxidants for PC12 cells

目的:研究囊泡单胺类转运体(VMAT)功能抑制对大鼠嗜铬瘤(PC12)细胞产生的内源性毒性及抗氧化剂的保护作用。方法:用流式细胞仪观察VMAT功能抑制以及不同干预方法对PC12细胞存活的影响和细胞死亡方式。结果:单独加入VMAT抑制剂利血平对PC12细胞无毒性作用;利血平协同多巴胺明显增加多巴胺的毒性,使同样浓度的多巴胺诱发PC12细胞的凋亡率明显增加。加入还原型谷胱甘肽(GSH)、二硫苏糖醇(DTT)和脉冲1号使PC12细胞的生存率明显提高。结论:VMAT功能抑制触发了多巴胺内源性毒性可诱发细胞凋亡,具有抗氧化作用的制剂有细胞保护作用。

Objective: To study the function inhibition of vesicular monoamine transporter (VMAT) on the protective role of endogenous toxicity and antioxidants for PC12 cells in rats. Methods: Flow cytometer were used to observe the function inhibition of VMAT and the influence on the survival of PC12 cells as well as their death way with different intervention methods. Results; Reserpine, an inhibitor of VMAT, itself had no poisonous effect on PC12 cells. Proserpine combined with dopamine could significantly increase the toxicity of dopamine, and the apoptosis ratio of PC12 cells induced by the same concentration of dopamine could significantly increase. Adding glutathione (GSH), dithiothreitol (DTT) and pulse number 1 could significantly increase the survival rate of PC12 cells. Conclusion: The function inhibition of VMAT triggers the endogenous toxicity of dopamine, which can induce the apoptosis and the mechanism of antioxidant action, and it has the function of cell protection.