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

To examine the effect of neuropeptide Y (NPY) on TGF-beta1 production in RAW264.7 macrophages.Enzyme linked immunosorbent assay (ELISA) was used to detect TGF-beta1 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.NPY treatment could promote TGF-beta1 production and rapid phosphorylation of PI3K p85 in RAW264.7 cells via Y1 receptor. The elevated TGF-beta1 production induced by NPY could be abolished by wortmannin pretreatment.NPY may elicit TGF-beta1 production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.