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白术内酯II通过激活Nrf2-ARE通路对乳腺肿瘤发生的化学预防作用。

Chemopreventive effects of atractylenolide II on mammary tumorigenesis via activating Nrf2-ARE pathway.

作者信息

Wang Ting, Long Fangyi, Zhang Xiqian, Yang Yujie, Jiang Xuehua, Wang Ling

机构信息

Department of Clinical Pharmacy and Pharmacy Administration, Key Laboratory of Drug Ministry of Education, West China School of Pharmacy, Sichuan University, Chengdu 610041, Sichuan, China.

Department of Pharmacy, Sichuan Cancer Hospital & Institution, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610041, China.

出版信息

Oncotarget. 2017 Aug 24;8(44):77500-77514. doi: 10.18632/oncotarget.20546. eCollection 2017 Sep 29.

DOI:10.18632/oncotarget.20546
PMID:29100404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5652796/
Abstract

In the studies of chemoprevention, the Nrf2-ARE signaling pathway has received widespread attention due to its anti-inflammatory and anti-oxidation effects. Our previous study indicated that atractylenolide II, which is an active component of , is a potential activator of Nrf2-ARE signaling pathway. In this study, we observed that atractylenolide II significantly increased Nrf2 expressing, nuclear translocation and the expression of its downstream detoxifying enzymes, thus decreasing 17β-Estradiol induced malignant transformation in MCF 10A cells, and we found that atractylenolide II acted through JNK/ERK-Nrf2-ARE pathway. Furthermore, atractylenolide II significantly reduced N-Nitroso-N-methylurea induced tumor incidence, multiplicity and volume, with activation of Nrf2-ARE pathway and decreased inflammation and oxidative stress in rat mammary tissue. Collectively, our results suggested that atractylenolide II could protect against mammary tumorigenesis both and via activating Nrf2-ARE signaling pathway, which supported atractylenolide II as a novel chemopreventive agent of breast cancer.

摘要

在化学预防研究中，Nrf2-ARE信号通路因其抗炎和抗氧化作用而受到广泛关注。我们之前的研究表明，白术内酯II作为[此处原文缺失相关成分]的活性成分，是Nrf2-ARE信号通路的潜在激活剂。在本研究中，我们观察到白术内酯II显著增加Nrf2的表达、核转位及其下游解毒酶的表达，从而减少17β-雌二醇诱导的MCF 10A细胞恶性转化，并且我们发现白术内酯II通过JNK/ERK-Nrf2-ARE途径发挥作用。此外，白术内酯II显著降低N-亚硝基-N-甲基脲诱导的大鼠乳腺肿瘤发生率、肿瘤数量和肿瘤体积，激活Nrf2-ARE途径并减轻大鼠乳腺组织中的炎症和氧化应激。总体而言，我们的结果表明白术内酯II可通过激活Nrf2-ARE信号通路预防[此处原文缺失相关内容]和[此处原文缺失相关内容]的乳腺肿瘤发生，这支持白术内酯II作为一种新型的乳腺癌化学预防剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/48799b939cb8/oncotarget-08-77500-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/a843d6253be5/oncotarget-08-77500-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/9ca50d305e72/oncotarget-08-77500-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/bfd5517bd4fa/oncotarget-08-77500-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/7a6ddcfd69cd/oncotarget-08-77500-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/8390b721873d/oncotarget-08-77500-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/8c9c88793fa3/oncotarget-08-77500-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/64489ac640fb/oncotarget-08-77500-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/48799b939cb8/oncotarget-08-77500-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/a843d6253be5/oncotarget-08-77500-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/9ca50d305e72/oncotarget-08-77500-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/bfd5517bd4fa/oncotarget-08-77500-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/7a6ddcfd69cd/oncotarget-08-77500-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/8390b721873d/oncotarget-08-77500-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/8c9c88793fa3/oncotarget-08-77500-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/64489ac640fb/oncotarget-08-77500-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148c/5652796/48799b939cb8/oncotarget-08-77500-g008.jpg

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