Jiang-Rui Zhou1, Zheng Xu, Chun-Lei Jiang. 1. Department of Nautical Medicine, Laboratory of Stress Medicine, Second Military Medical University, Shanghai, China.
Abstract
OBJECTIVE: To examine the effect of neuropeptide Y (NPY) on TGF-beta1 production in RAW264.7 macrophages. METHODS: 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. RESULTS: 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. CONCLUSION: NPY may elicit TGF-beta1 production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.
OBJECTIVE: To examine the effect of neuropeptide Y (NPY) on TGF-beta1 production in RAW264.7 macrophages. METHODS: 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. RESULTS: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. CONCLUSION:NPY may elicit TGF-beta1 production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.
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