Morroniside alleviates lipopolysaccharide-induced inflammatory and oxidative stress in inflammatory bowel disease by inhibiting NLRP3 and NF-κB signaling pathways.

Abstract

To investigate the effects of morroniside on inflammatory and oxidative stress in lipopolysaccharide (LPS)-induced inflammatory bowel disease (IBD) cell model. NCM460 cells were treated with 2-, 5-, or 10-μg/mL LPS for 24 h to develop an IBD cell model. MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) colorimetric assay was performed to uncover the role of morroniside on the viability of LPS-treated NCM460 cells. Flow cytometry and immunoblot assays were performed to confirm the effects of morroniside on the apoptosis of LPS-treated NCM460 cells. Quantitative polymerase chain reaction and enzyme-linked-immunosorbent serologic assays were performed to confirm the effects of morroniside on inflammatory and oxidative stress by measuring the levels of tumor necrosis factor-α, interleukin-1β, IL-6, superoxide dismutase, malondialdehyde, total antioxidant capacity, and myeloperoxidase. In addition, immunoblot and immunofluorescence assays were performed to detect the effects of morroniside on NLRP3 and NF-κB pathways. Monosine attenuated LPS-induced injury of NCM460 cells. Monosine reduced LPS-induced inflammation in NCM460 cells. In addition, morroniside reduced LPS-induced oxidative stress in NCM460 cells. Mechanically, morroniside suppressed NLRP3 and NF-κB pathways, and alleviated LPS-induced inflammatory and oxidative stress in IBD. Morroniside could serve as a promising drug for treating IBD.