Camellia nitidissima Chi extract ameliorates dextran sulfate sodium-induced acute ulcerative colitis in mice by inhibiting TLR4/NF-κB-mediated inflammatory activation.

Abstract

Camellia nitidissima Chi (CNC), whose main composition was gallic acid, catechin, procyanidin-gallate, apigenin-pentosyl-glucoside, vitexin, cyanidin-3-o-glucoside, myricitrin-glucoside, gallocatechin-gallate, epicatechin and rutin, posses sound anti-inflammatory and antioxidant effects. This study aimed to explore the protective effects and mechanisms of the alcoholic extract of CNC on dextran sulfate sodium-induced ulcerative colitis. CNC effectively maintained weight and colon length, and significantly ameliorated colonic histopathological damage. Furthermore, CNC mitigated colitis-induced oxidative stress and exhibited anti-inflammatory properties in UC mice by reducing levels of myeloperoxidase (MPO) and malondialdehyde (MDA), decreasing the production of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). In addition, CNC downregulated the protein expression levels of TLR4, p-NF-κBP65, and p-IκBα of the inflammation-related TLR4/NF-κB signaling pathways. Validation of the molecular docking results also revealed that rutin, the most abundant compound in CNC, interacts with TLR4 and NF-κB protein mainly through hydrogen bonds. CNC also promoted the proliferation of Lactobacillus and Bifidobacterium while reducing the number of Enterococcus, E. coli, Bacteroides, and Peptococcus in mice to improve the intestinal environment and alleviate colitis. CNC inhibited TLR4/NF-κB signaling pathways to relieve inflammation and oxidative damage on UC, is a potential development of natural medicine for UC.