The Ethanol Extract of Licorice (Glycyrrhiza uralensis) Protects against Triptolide-Induced Oxidative Stress through Activation of Nrf2.

The Ethanol Extract of Licorice (Glycyrrhiza uralensis) Protects against Triptolide-Induced Oxidative Stress through Activation of Nrf2.
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甘草乙醇提取物通过激活 Nrf2 防止雷公藤甲素诱导的氧化应激

DOI:
10.1155/2017/2752389
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发表时间:
2017
期刊:
Evidence-based complementary and alternative medicine : eCAM
影响因子:
--
通讯作者:
Yan M
Yan M
中科院分区:
其他
文献类型:
--
作者:
Cao LJ;Hou ZY;Li HD;Zhang BK;Fang PF;Xiang DX;Li ZH;Gong H;Deng Y;Ma YX;Tang HB;Yan M

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为探讨甘草乙醇提取物(LEE)中核因子红细胞2相关因子2(Nrf 2)对雷公藤甲素(TP-)诱导的肝毒性的潜在作用,将HepG 2细胞暴露于LEE(30、60和90 mg·L-1)12 h,然后用TP(50 nM)处理24 h。此外,ICR小鼠腹腔注射TP(1.0 mg·kg-1)建立急性肝损伤模型。相关的氧化剂和抗氧化介质进行了分析。TP导致HepG 2细胞明显的氧化应激,表现为ROS水平升高和GSH含量降低。体外结果可能适用于体内实验。LEE在体外和体内条件下均能保护TP诱导的氧化应激。此外,在TP处理组中观察到Nrf 2水平降低。下游基因的mRNA水平在ICR小鼠肝脏中也下降,而在HepG 2细胞中则增加。与此相反,LEE预处理显着增加Nrf 2及其下游基因的水平。LEE部分通过激活Nrf 2途径保护TP诱导的氧化应激。
To investigate the potential role of nuclear factor erythroid 2-related factor 2 (Nrf2) in licorice ethanol extract (LEE) against triptolide- (TP-) induced hepatotoxicity, HepG2 cells were exposed to LEE (30, 60, and 90 mg·L−1) for 12 h and then treated with TP (50 nM) for 24 h. Besides, an acute liver injury model was established in ICR mice by a single dose of TP (1.0 mg·kg−1, i.p.). Relevant oxidant and antioxidant mediators were analyzed. TP led to an obvious oxidative stress as evidenced by increasing levels of ROS and decreasing GSH contents in HepG2 cells. In vitro results were likely to hold true in in vivo experiments. LEE protected against TP-induced oxidative stress in both in vitro and in vivo conditions. Furthermore, the decreased level of Nrf2 in the TP-treated group was observed. The mRNA levels of downstream genes decreased as well in ICR mice liver, whereas they increased in HepG2 cells. In contrast, LEE pretreatment significantly increased the level of Nrf2 and its downstream genes. LEE protects against TP-induced oxidative stress partly via the activation of Nrf2 pathway.
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