肝胆相照论坛

标题: 齐墩果酸重新编程肝脏以防止肝毒性,但在高剂量时具有肝 [打印本页]

作者: StephenW    时间: 2018-8-9 11:35     标题: 齐墩果酸重新编程肝脏以防止肝毒性,但在高剂量时具有肝

Reviews
Oleanolic acid reprograms the liver to protect against hepatotoxicants, but is hepatotoxic at high doses
Jie Liu
Yuan‐Fu Lu
Qin Wu
Shang‐Fu Xu
Fu‐Guo Shi
Curtis D. Klaassen
First published: 06 August 2018
https://doi.org/10.1111/liv.13940

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/liv.13940


Abstract

Oleanolic acid (OA) is a triterpenoid that exists widely in fruits, vegetables, and medicinal herbs. OA is included in some dietary supplements and is used as a complementary and alternative medicine (CAM) in China, India, Asia, the US and European countries. OA is effective in protecting against various hepatotoxicants, and one of the protective mechanisms is reprograming the liver to activate the nuclear factor erythroid 2‐related factor 2 (Nrf2). OA derivatives, such as CDDO‐Im and CDDO‐Me, are even more potent Nrf2 activators. OA has recently been shown to also activate the Takeda G‐protein coupled receptor (TGR5). However, whereas a low dose of OA is hepatoprotective, higher doses and long‐term use of OA can produce liver injury, characterized by cholestasis. This paradoxical hepatotoxic effect occurs not only for OA, but also for other OA‐type triterpenoids. Dose and length of time of OA exposure differentiate the ability of OA to produce hepatoprotection versus hepatotoxicity. Hepatotoxicity produced by herbs is increasingly recognized and is of global concern. Given the appealing nature of OA in dietary supplements and its use as an alternative medicine around the world, as well as the development of OA derivatives (CDDO‐Im and CDDO‐Me) as therapeutics, it is important to understand not only that they program the liver to protect against hepatotoxic chemicals, but also how they produce hepatotoxicity.

This article is protected by copyright. All rights reserved.

作者: StephenW    时间: 2018-8-9 11:36

评测
齐墩果酸重新编程肝脏以防止肝毒性,但在高剂量时具有肝毒性
刘杰
袁福禄
秦武
徐尚福
傅国石
柯蒂斯D.克拉森
首次发布:2018年8月6日
https://doi.org/10.1111/liv.13940

本文已被接受发布并经过完整的同行评审,但尚未通过编辑,排版,分页和校对过程,这可能导致此版本与记录版本之间存在差异。请引用本文作为doi:10.1111 / liv.13940


抽象

齐墩果酸(OA)是一种三萜类化合物,广泛存在于水果,蔬菜和药材中。 OA包含在一些膳食补充剂中,并在中国,印度,亚洲,美国和欧洲国家用作补充和替代药物(CAM)。 OA在防止各种肝毒性方面是有效的,并且保护机制之一是重新编程肝脏以激活核因子红细胞2相关因子2(Nrf2)。 OA衍生物,如CDDO-Im和CDDO-Me,是更有效的Nrf2激活剂。最近已显示OA也激活武田G蛋白偶联受体(TGR5)。然而,尽管低剂量的OA具有保肝作用,但较高剂量和长期使用OA可产生以胆汁淤积为特征的肝损伤。这种矛盾的肝毒性作用不仅发生在OA,还发生在其他OA型三萜类化合物中。 OA暴露的剂量和时间长度区分OA产生肝保护与肝毒性的能力。草药产生的肝毒性越来越受到人们的认可,并引起全球关注。鉴于膳食补充剂中OA的吸引力及其作为世界各地的替代药物的用途,以及OA衍生物(CDDO-Im和CDDO-Me)作为治疗剂的开发,重要的是不仅要了解它们的程序肝脏可以预防肝毒性化学物质,还可以产生肝毒性。

本文受版权保护。版权所有。




欢迎光临 肝胆相照论坛 (http://hbvhbv.info/forum/) Powered by Discuz! X1.5