6-shogaol-rich extract from ginger up-regulates the antioxidant defense systems in cells and mice.

6-shogaol-rich extract from ginger up-regulates the antioxidant defense systems in cells and mice.
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姜的6个shogaol提取物上调细胞和小鼠的抗氧化剂防御系统。

DOI:
10.3390/molecules17078037
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发表时间:
2012-07-04
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
通讯作者:
Jeong WS
Jeong WS
中科院分区:
其他
文献类型:
--
作者:
Bak MJ;Ok S;Jun M;Jeong WS

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众所周知,生姜的根茎(Zingiber officinale Roscoe)含有几种生物活性化合物,包括姜辣素和姜酚,它们具有有益的健康特性,如抗炎和化学预防作用。基于最近对6-shogaol可能比6-姜辣素具有更强生物活性的观察,我们从生姜中提取了富含6-shogaol的提取物,并在体外和体内研究了其对核因子e2相关因子2 (Nrf2)/抗氧化反应元件(ARE)途径的影响。生姜粉在80℃干燥后,用95%乙醇在80℃下提取,得到6- shogaol富提取物(GEE8080)。GEE8080的6-shogaol含量是常温提取液(GEE80RT)的6倍以上。在HepG2细胞中,GEE8080对are报告基因活性和Nrf2表达的诱导作用比GEE80RT强得多。GEE8080刺激有丝分裂原活化蛋白激酶(MAPKs)如ERK、JNK和p38的磷酸化。此外,用SB202190 (p38特异性抑制剂)和LY294002 (Akt特异性抑制剂)处理gee8080诱导的Nrf2和HO-1表达减弱。在小鼠模型中,GEE8080降低了二乙基亚硝胺(DEN)介导的血清天冬氨酸转氨酶和丙氨酸转氨酶升高以及DEN诱导的肝脂质过氧化。GEE8080对Nrf2和HO-1的诱导作用也在小鼠中得到证实。此外,小鼠给药GEE8080也恢复了den降低的肝脏抗氧化酶如超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶的活性和蛋白质表达。综上所述,富含6-shogaol的生姜提取物GEE8080可能在体内外通过诱导p38 MAPK和PI3k/Akt通路调控的Nrf2和HO-1增强抗氧化防御机制。
The rhizome of ginger (Zingiber officinale Roscoe) is known to have several bioactive compounds including gingerols and shogaols which possess beneficial health properties such as anti-inflammatory and chemopreventive effects. Based on recent observations that 6-shogaol may have more potent bioactivity than 6-gingerol, we obtained a 6-shogaol-rich extract from ginger and examined its effects on the nuclear factor E2-related factor2 (Nrf2)/antioxidant response element (ARE) pathway in vitro and in vivo. 6-Shogaol-rich extract was produced by extracting ginger powder with 95% ethanol at 80 °C after drying at 80 °C (GEE8080). GEE8080 contained over 6-fold more 6-shogaol compared to the room temperature extract (GEE80RT). In HepG2 cells, GEE8080 displayed much stronger inductions of ARE-reporter gene activity and Nrf2 expression than GEE80RT. GEE8080 stimulated phosphorylations of mitogen-activated protein kinases (MAPKs) such as ERK, JNK, and p38. Moreover, the GEE8080-induced expressions of Nrf2 and HO-1 were attenuated by treatments of SB202190 (a p38 specific inhibitor) and LY294002 (an Akt specific inhibitor). In a mouse model, the GEE8080 decreased the diethylnitrosamine (DEN)-mediated elevations of serum aspartate transaminase and alanine transaminase as well as the DEN-induced hepatic lipid peroxidation. Inductions of Nrf2 and HO-1 by GEE8080 were also confirmed in the mice. In addition, the administration of GEE8080 to the mice also restored the DEN-reduced activity and protein expression of hepatic antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and catalase. In conclusion, GEE8080, a 6-shogaol-rich ginger extract, may enhance antioxidant defense mechanism through the induction of Nrf2 and HO-1 regulated by p38 MAPK and PI3k/Akt pathway in vitro and in vivo.
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