Neuropeptide Y promotes TGF-β1 production in RAW264.7 cells by activating PI3K pathway via Y1 receptor Translated title: 神经肽Y通过Y1受体激活PI3K通路促进RAW264.7细胞中TGF-β1 的产生 周江睿, 徐拯, 蒋春雷

Abstract

Objective

To examine the effect of neuropeptide Y (NPY) on TGF-β1 production in RAW264.7 macrophages.

Methods

Enzyme linked immunosorbent assay (ELISA) was used to detect TGF-β1 production. Cell counting kit 8 (CCK-8) was used to assay the viability of RAW264.7 cells. Western blot was used to detect the phosphorylation of PI3K p85.

Results

NPY treatment could promote TGF-β1 production and rapid phosphorylation of PI3K p85 in RAW264.7 cells via Y1 receptor. The elevated TGF-β1 production induced by NPY could be abolished by wortmannin pretreatment.

Conclusion

NPY may elicit TGF-β1 production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.

摘要

目的

探讨神经肽Y对巨噬细胞系RAW264.7分泌转化生长因子TGF-β1的影响。

方法

酶联免疫吸附实验检测细胞培养上清液中的TGF-β1 水平; 细胞计数试剂盒CCK-8 检测细胞活力; Western blot 检测磷脂酰肌醇3 激酶PI3K p85的磷酸化水平。

结果

神经肽Y主要通过激活其Y1受体信号通路增加RAW264.7细胞中TGF-β1的产生, 并可在10 min内快速激活PI3K通路。 PI3K通路阻滞剂可消除NPY 对TGF-β1产生的促进作用。

结论

神经肽Y能够通过Y1 受体促进RAW264.7 细胞的TGF-β1 的表达, 此作用可能由PI3K介导。