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新型合成类黄酮衍生物GL-V9通过激活AMPK/FOXO3a途径上调Trx-1表达，减轻DSS诱导的结肠炎氧化应激。

GL-V9, a new synthetic flavonoid derivative, ameliorates DSS-induced colitis against oxidative stress by up-regulating Trx-1 expression via activation of AMPK/FOXO3a pathway.

作者信息

Zhao Yue, Sun Yang, Ding Youxiang, Wang Xiaoping, Zhou Yuxin, Li Wenjun, Huang Shaoliang, Li Zhiyu, Kong Lingyi, Guo Qinglong, Lu Na

机构信息

State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, Jiangsu Key Laboratory of Drug Design and Optimization, China Pharmaceutical University, Nanjing 210009, China.

School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China.

出版信息

Oncotarget. 2015 Sep 22;6(28):26291-307. doi: 10.18632/oncotarget.4657.

DOI:10.18632/oncotarget.4657
PMID:26327408
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4694902/
Abstract

GL-V9, a new synthesized flavonoid derivative, has been reported to possess anti-cancer properties in our previous studies. Uncontrolled overproduction of reactive oxygen species (ROS) has been implicated in oxidative damage of inflammatory bowel disease (IBD). In this study, we aimed to investigate the protective effect of GL-V9 against dextran sulfate sodium (DSS)-induced colitis. GL-V9 attenuated DSS-induced body weight loss, colon length shortening and colonic pathological damage. GL-V9 also inhibited inflammatory cells infiltration and decreased myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) activities. Moreover, GL-V9 inhibited ROS and malondialdehyde (MDA) generation, but enhanced superoxide dismutase (SOD), glutathione (GSH) and total antioxidant capacity. GL-V9 reduced pro-inflammatory cytokines production in serum and colon as well. Mechanically, GL-V9 could increase Trx-1 via activation of AMPK/FOXO3a to suppress DSS-induced colonic oxidative stress. Furthermore, GL-V9 decreased pro-inflammatory cytokines and ROS production and increased the antioxidant defenses in the mouse macrophage cells RAW264.7 by promoting Trx-1 expression. In conclusion, our study demonstrated that GL-V9 attenuated DSS-induced colitis against oxidative stress by up-regulating Trx-1 via activation of AMPK/FOXO3a pathway, suggesting that GL-V9 might be a potential effective drug for colitis.

摘要

GL-V9是一种新合成的黄酮类衍生物，在我们之前的研究中已报道其具有抗癌特性。活性氧（ROS）的失控过度产生与炎症性肠病（IBD）的氧化损伤有关。在本研究中，我们旨在研究GL-V9对葡聚糖硫酸钠（DSS）诱导的结肠炎的保护作用。GL-V9减轻了DSS诱导的体重减轻、结肠长度缩短和结肠病理损伤。GL-V9还抑制了炎症细胞浸润，并降低了髓过氧化物酶（MPO）和诱导型一氧化氮合酶（iNOS）的活性。此外，GL-V9抑制了ROS和丙二醛（MDA）的产生，但增强了超氧化物歧化酶（SOD）、谷胱甘肽（GSH）和总抗氧化能力。GL-V9还降低了血清和结肠中促炎细胞因子的产生。机制上，GL-V9可通过激活AMPK/FOXO3a增加Trx-1，以抑制DSS诱导的结肠氧化应激。此外，GL-V9通过促进Trx-1表达，降低了小鼠巨噬细胞RAW264.7中促炎细胞因子和ROS的产生，并增强了抗氧化防御能力。总之，我们的研究表明，GL-V9通过激活AMPK/FOXO3a途径上调Trx-1，减轻了DSS诱导的结肠炎氧化应激，提示GL-V9可能是一种治疗结肠炎的潜在有效药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/ba225cd9ef1c/oncotarget-06-26291-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/7a2689279b2a/oncotarget-06-26291-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/fe96141149b7/oncotarget-06-26291-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/bb6a2a4a9f44/oncotarget-06-26291-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/e2e0b8f622be/oncotarget-06-26291-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/ba225cd9ef1c/oncotarget-06-26291-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/7a2689279b2a/oncotarget-06-26291-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/e5941d878643/oncotarget-06-26291-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/358fabf2ac00/oncotarget-06-26291-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/9a480b813e6c/oncotarget-06-26291-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/fe96141149b7/oncotarget-06-26291-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/bb6a2a4a9f44/oncotarget-06-26291-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/e2e0b8f622be/oncotarget-06-26291-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87d1/4694902/ba225cd9ef1c/oncotarget-06-26291-g008.jpg

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