%0 Journal Article
%T Rutin mitigates acetic acid-induced ulcerative colitis: novel coloprotective mechanism.
%A Sherif IO
%A Al-Shaalan NH
%A Awadin WF
%J Toxicol Res (Camb)
%V 13
%N 4
%D 2024 Aug
%M 39119265
%F 2.68
%R 10.1093/toxres/tfae108
%X UNASSIGNED: Ulcerative colitis, an inflammatory bowel disease, is characterized by a status of oxidative stress and inflammation. Rutin is a natural flavonoid with many pharmacological activities and its role in acetic acid-induced ulcerative colitis through the high mobility group B1 (HMGB1)/ toll-like receptor-4 (TLR4)/ myeloid differentiation primary response protein 88 (MYD88)/ nuclear factor-kB (NF-kB) signaling pathway needs to be explored.
UNASSIGNED: Four experimental groups were divided into control group, rutin group: treated with 100 mg/kg/day rutin orally for 10 days, acetic acid (AA) group: given intracolonic instillation of AA to induce ulcerative colitis, and acetic acid with rutin treatment (AA/Rutin) group.
UNASSIGNED: Acetic acid caused a marked increase in the colon weight/length ratio and induced colonic histopathological changes, leading to a marked rise in the colonic histopathological scores. Acetic acid exhibited a significant rise in LDH and CRP serum levels as well as TOS colonic levels, accompanied by a marked decline in TAS colonic contents compared to the control group. Moreover, AA-induced activation of the HMGB1/TLR4/MYD88/NF-kB signaling pathway. Rutin demonstrated a significant decrease in the colon weight/length ratio, ameliorated the colonic histopathological changes induced by AA, and exhibited a marked decline in the colonic histopathological scores. Rutin showed a significant decrease in serum LDH, and CRP levels as well as colonic TOS contents when compared with the AA group. Rutin suppressed the colonic activation of the HMGB1/TLR4/MYD88/NF-kB signaling pathway.
UNASSIGNED: Rutin could be a promising coloprotective agent against AA-induced ulcerative colitis by targeting the HMGB1/TLR4/MYD88/NF-kB signaling pathway.