PDF(Pubmed)
Abstract：
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.
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.
摘要：
■溃疡性结肠炎，炎症性肠病,以氧化应激和炎症状态为特征。芦丁是一种具有多种药理活性的天然黄酮类化合物,其通过高迁移率族B1(HMGB1)/Toll样受体-4(TLR4)/髓样分化原发反应蛋白88(MYD88)/核因子-kB(NF-kB)信号通路在醋酸诱导的溃疡性结肠炎中的作用有待探索。
■将四个实验组分为对照组，芦丁组：100mg/kg/天口服芦丁治疗10天，乙酸（AA）组：给予结肠内滴注AA诱导溃疡性结肠炎，乙酸与芦丁处理(AA/芦丁)组。
■乙酸引起结肠重量/长度比的显着增加，并引起结肠组织病理学变化，导致结肠组织病理学评分显著上升。乙酸显示LDH和CRP血清水平以及TOS结肠水平显着升高，与对照组相比，TAS结肠含量显着下降。此外，AA诱导HMGB1/TLR4/MYD88/NF-kB信号通路的激活.芦丁显示结肠重量/长度比显著降低，改善了AA引起的结肠组织病理学变化，结肠组织病理学评分明显下降。芦丁显示血清LDH显著降低，与AA组相比，CRP水平以及结肠TOS含量。芦丁抑制HMGB1/TLR4/MYD88/NF-kB信号通路的结肠活化。
■芦丁通过靶向HMGB1/TLR4/MYD88/NF-kB信号通路，可能成为抗AA诱导的溃疡性结肠炎的有前途的保生剂。
■将四个实验组分为对照组，芦丁组：100mg/kg/天口服芦丁治疗10天，乙酸（AA）组：给予结肠内滴注AA诱导溃疡性结肠炎，乙酸与芦丁处理(AA/芦丁)组。
■乙酸引起结肠重量/长度比的显着增加，并引起结肠组织病理学变化，导致结肠组织病理学评分显著上升。乙酸显示LDH和CRP血清水平以及TOS结肠水平显着升高，与对照组相比，TAS结肠含量显着下降。此外，AA诱导HMGB1/TLR4/MYD88/NF-kB信号通路的激活.芦丁显示结肠重量/长度比显著降低，改善了AA引起的结肠组织病理学变化，结肠组织病理学评分明显下降。芦丁显示血清LDH显著降低，与AA组相比，CRP水平以及结肠TOS含量。芦丁抑制HMGB1/TLR4/MYD88/NF-kB信号通路的结肠活化。
■芦丁通过靶向HMGB1/TLR4/MYD88/NF-kB信号通路，可能成为抗AA诱导的溃疡性结肠炎的有前途的保生剂。
