咖啡酸苯乙酯
镉
细胞凋亡
PI3K/AKT/mTOR通路
化学
药理学
氧化应激
蛋白激酶B
TLR4型
海角
炎症
咖啡酸
生物化学
医学
内科学
抗氧化剂
信号转导
有机化学
考古
历史
作者
Rili Hao,Junlin Ge,Yuan Ren,Xubin Song,Yang Jiang,Dongxiao Sun‐Waterhouse,Feng Li
标识
DOI:10.1016/j.ecoenv.2020.111578
摘要
Cadmium (Cd), an environmental pollutant, is evidenced to cause hepatotoxicity. In this study, the potential protective effect of caffeic acid phenethyl ester (CAPE) on cadmium-induced liver damage was investigated. Forty male mice were treated daily with either CdCl2 (1.5 mg/kg body weight (b.w.), gavage) or CAPE (10 μmol/kg b.w., gavage) or both for 4 weeks. CAPE administration significantly reduced Cd level and liver and body weight, and increased AST, ALT and ALP level. Moreover, CAPE prevented CdCl2-induced oxidative stress via PI3K/Akt/mTOR pathway and inhibited apoptosis by regulating apoptosis markers. CAPE also suppressed the CdCl2-induced inflammation by reducing the inflammatory mediators, including TNF-α, IL-6 and IL-1β. Furthermore, CAPE alleviated CdCl2-induced reduction of TLR4. It should be noted that this effect was achieved by targeting miR-182-5p, and CAPE improved miR-182-5p level. The improvement of the liver tissue histopathology by CAPE confirmed the biochemical data. These results show for the first time that miR-182-5p/TLR4 axis involved in CAPE's protection against CdCl2-induced hepatotoxicity, and may provide novel insights into the treatment of cadmium-related diseases.
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