Neferine, a natural alkaloid from Nelumbo nucifera, ameliorates experimental chronic ulcerative colitis in mice

• Main Authors: Xiangjing Min (Author), Yishan Zhou (Author), Shuangli Xiang (Author), Rong Sun (Author), Qin Wu (Author), Jingshan Shi (Author), Xiuping Chen (Author)
• Format: Book
• Published: Elsevier, 2021-12-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 2667-1425; 10.1016/j.prmcm.2021.100022
• Keywords: Neferine; Chronic ulcerative colitis; Cytokine; NF-κB; Other systems of medicine; RZ201-999; Therapeutics. Pharmacology; RM1-950
• Source: Pharmacological Research - Modern Chinese Medicine, Vol 1, Iss , Pp 100022- (2021)

Objective: Ulcerative colitis (UC), a chronic inflammatory disease, is closely associated with the development of colorectal cancer. Neferine is a natural alkaloid that possesses many therapeutic effects. Our previous studies showed that neferine showed a significant protective effect on the acute ulcerative colitis mouse model. Here, the protective role of neferine on chronic UC was investigated. Methods: A chronic mice UC model was established by employing dextran sodium sulfate (DSS) and neferine was orally administrated. The disease activity index (DAI) scores were calculated. The levels of pro-inflammatory mediators were determined by ELISA kits. The pathological changes were evaluated by H&E staining. Protein expressions were detected by immunohistochemistry and Western blotting. Results: Neferine treatment significantly decreased the DAI scores, ameliorated pathological injuries, and reduced the levels of myeloperoxidase (MPO), IL-1β, IL-6, and TNF-α. Furthermore, the expressions of NF-κB p65, receptor-interacting protein kinase 1 and 3 (RIP1 and RIP3), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in colon tissues were suppressed by neferine. In addition, the decreased expression of caspase-8 and IκBα were restored by neferine. Conclusion: Neferine protects chronic UC by regulating the secretion of pro-inflammatory cytokines and inhibiting the NF-κB signaling pathway.