脂多糖
下调和上调
结肠炎
肝损伤
GPX4
抗氧化剂
细胞因子
化学
谷胱甘肽
肿瘤坏死因子α
溃疡性结肠炎
药理学
免疫学
医学
酶
超氧化物歧化酶
生物化学
内科学
谷胱甘肽过氧化物酶
基因
疾病
作者
Yonger Chen,Shumin Zhu,Zongwen Chen,Ying Liu,Chaoying Pei,Haiyang Huang,Shaozhen Hou,Weimin Ning,Jian Liang
标识
DOI:10.1021/acs.jafc.2c05262
摘要
in the liver were detected by kits. Cytokine levels (TNF-α, IL-1β, and IL-6) and Gpx4 activity in the liver were detected by ELISA. Finally, the activation of nuclear factor erythroid 2-like 2 (Nrf2) was detected to explore the mechanism. The results indicated that GA significantly attenuated DSS-induced hepatic pathological damage, liver parameters, and cytokine levels and increased the antioxidant enzyme activities. Moreover, GA attenuated ferroptosis in DSS-induced liver injury and upregulated Gpx4 expression in DSS-induced mice. Mechanistic experiments revealed that GA activated Nrf2 in mice. Taken together, this study demonstrates that GA can alleviate ferroptosis in SLI in DSS-induced colitis mice, and its protective effects are associated with activating the Nrf2-Gpx4 signaling pathway.
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