Procyanidin A2 penetrates L-02 cells and protects against tert-butyl hydroperoxide-induced oxidative stress by activating Nrf2 through JNK and p38 phosphorylation

Procyanidin A2 penetrates L-02 cells and protects against tert-butyl hydroperoxide-induced oxidative stress by activating Nrf2 through JNK and p38 phosphorylation
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原花青素 A2 渗透 L-02 细胞,通过 JNK 和 p38 磷酸化激活 Nrf2,防止叔丁基过氧化氢诱导的氧化应激

DOI:
10.1016/j.jff.2019.103562
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发表时间:
2019-11
影响因子:
5.6
通讯作者:
Chao-Mei Ma
Chao-Mei Ma
中科院分区:
农林科学2区
文献类型:
--
作者:
Hai-Yan Xu;Xin-Hong Feng;Peng-Fei Zhao;Alatangaole Damirin;Chao-Mei Ma

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我们研究了原花青素A2(PA 2)对人胎肝细胞系(L-02)氧化应激的保护作用,及其调节细胞抗氧化反应中的关键因子-核因子红细胞2相关因子2(Nrf 2)的机制。PA 2可保护L-02细胞免受叔丁基过氧化氢诱导的氧化损伤,表现为细胞活力增加,乳酸脱氢酶释放和细胞内活性氧产生减少。PA 2促进Nrf 2的核转位并上调血红素加氧酶-1和NAD(P)H醌氧化还原酶1。此外,c-Jun N-末端激酶和p38 MAP激酶信号通路被PA 2激活。PA 2以二聚体形式穿透L-02细胞,胞质浓度在24 h达到峰值,晚于黄烷-3-醇单体。PA 2经口给药后可被吸收到血浆中并分布到肝脏。
We examined the protective effects of procyanidin A2 (PA2) against oxidative stress in a human fetal hepatocyte line (L-02), and its mechanism with respect to regulating nuclear factor erythroid 2-related factor 2 (Nrf2), a key factor in the cellular antioxidant response. PA2 protected L-02 cells from oxidative damage that was induced bytert-butyl hydroperoxide, as evidenced by the increase in cell viability and the reduction in lactate dehydrogenase release and intracellular reactive oxygen species production. PA2 promoted the nuclear translocation of Nrf2 and upregulated heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1. In addition, the c-Jun N-terminal kinase and p38 MAP kinase signaling pathways were activated by PA2. PA2 penetrated L-02 cells in dimeric form, with the cytosolic concentration peaking at 24 h, later than the flavan-3-ol monomers. PA2 can be absorbed into plasma and distributed to the liver after oral administration in mice.
二乙酰化和丙酮结合的 flavan-3-ols 作为具有细胞渗透能力的有效抗氧化剂
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