二十二碳五烯酸对PC12细胞神经突起生长的诱导作用

Effect of docosapentenoic acid on the neurite outgrowth in PC12 cells

目的探讨二十二碳五烯酸（docosapentenoicacid，DPA）对PCI2细胞神经突起生长的诱导作用。方法通过培养PCI2细胞，利用MoticZamgesPlus软件测绘细胞图像，观察不同浓度DPA对神经突起形成的影响；Western blot法检测神经元突起标志物βⅢ—tubulin的表达及细胞外调节蛋白激酶（ERK）和蛋白激酶B（Akt）磷酸化程度。结果P12细胞神经突起形成率在DPA的诱导下呈浓度依赖性增加，较对照组分别增加2．4％（DPA10μg／ml，P〉0．05）、18．6％（DPA30μg／ml，P〈0．05）和25．0％（DPA50μg／ml，P〈0．05）；DPA可促进pmtubulin的表达（P〈0．05），提高ERK与Akt的磷酸化水平（P〈0．05）。结论DPA促进PCI2细胞神经细胞突起生长，其机制可能与激活ERK和Akt信号通路有关。

Objective To explore the inductive action of docosapentenoic acid （DPA） on neurite outgrowth in PC12 cells in vitro. Methods Neurite outgrowth in PC12 cells was examined after the treatment with different concentration of DPA using Motic Zamges Plus software mapping cell image system. Western blot was performed to detect the expression of βⅢ-tubulin regulated protein kinase, a neuronal marker as well as ERK and protein kinase B （Akt） phosphorylation. Results PC12 cell neurite formation rate was increased in a concentration dependent manner in the induction of DPA, increased by 2.4% （ DPA 10 μg/ml,P〉0.05）, 18.6% （DPA 30 μg,/ml,P〈0.05） and 25.0% （DPA 50 μg/ml,P〈0.05） compared with that in the control group. DPA promoted the expression of βⅢ-tubulin （P〈0.05） and the phosphorylation level of ERK and Akt （P〈0.05,P〈0.01）. Conclusion DPA promotes PC12 cell neurites growth and its mechanism may be related to the activation of ERK and Akt signaling pathways.