N-(p-Coumaroyl) serotonin mitigates inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells and phorbol 12-myristate 13-acetate-stimulated A549 cells through NF-κB and MAPK inactivation.

Inflammation is a protective response of the body, but excessive inflammation can exacerbate conditions such as acute lung injury and asthma. N-(p-Coumaroyl) serotonin (CS) is known to have anti-inflammatory effects. The present study aimed to explore the anti-inflammatory effects of CS on lipopolysaccharide (LPS)-induced inflammatory responses in macrophages and lung epithelial cells. Cellular inflammatory responses and associated signaling pathways were analyzed using ELISA, Western blotting and immunocytochemistry. Initial increase in cytokine (including IL-6 and TNF-α) and chemokine [including monocyte chemoattractant protein-1 (MCP-1)] levels, nitric oxide formation and inducible NO synthase expression in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, was reduced by CS pretreatment. In addition, CS blocked LPS-induced MAPK/NF-κB activation in RAW264.7 cells. CS led to heme oxygenase-1 (HO-1) upregulation in RAW264.7 cells. In PMA-stimulated A549 lung epithelial cells, the increase in IL-6, TNF-α and MCP-1 expression was also attenuated by CS. This was accompanied by decreased MAPK/NF-κB activation. Furthermore, CS elevated the expression of HO-1 in A549 cells. Collectively, the present study confirmed that CS exhibited anti-inflammatory effects in both macrophages and lung epithelial cell lines, suggesting that CS may alleviate systemic or lung inflammation.