淫羊藿
化学
氧化应激
KEAP1型
药理学
TLR4型
自噬
PI3K/AKT/mTOR通路
脂多糖
安普克
炎症
信号转导
结肠炎
生物化学
激酶
生物
蛋白激酶A
免疫学
医学
中医药
病理
转录因子
细胞凋亡
替代医学
基因
作者
Linxian Zhao,Tao Jiang,Yuxin Zhang,Zhen Shen
摘要
BACKGROUND: Epimedium polysaccharide (EPS) is a bioactive compound derived from the traditional Chinese herb Epimedium brevicornum. The objective of this study was to investigate the protective effects of EPS on ulcerative colitis (UC) and to elucidate the underlying mechanisms involved. RESULTS: ) mice. Additionally, Western blotting and immunohistochemical analysis demonstrated that EPS facilitated autophagy via the adenosine monophosphate-dependent protein kinase/mammalian target of rapamycin (AMPK/mTOR) pathway. In vitro experiments revealed that EPS effectively suppressed lipopolysaccharide (LPS)-mediated cellular damage and oxidative stress by regulating Keap1/Nrf2 pathway. Transcriptomic analysis of LPS-treated Caco-2 cells following EPS treatment revealed a significant up-regulation of Nrf2 expression. CONCLUSION: In conclusion, the findings of this study suggest that EPS exerts protective effects against DSS-induced UC through the inhibition of the TLR4/NF-κB signaling pathway, regulation of the Keap1/Nrf2 pathway, and promotion of autophagy via the AMPK/mTOR pathway. Consequently, EPS may represent a potential therapeutic target for the treatment of UC. © 2024 Society of Chemical Industry.
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