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

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.