Palbinone from Paeonia suffruticosa Protects Hepatic Cells via Up-regulation of Heme Oxygenase-1

被引：10

作者：

Do Thi Ha ^{[1
,2
]}

Tran Thi Phuong ^{[3
]}

Oh, Joonseok ^{[4
,5
]}

Bae, KiHwan ^{[2
]}

Nguyen Duy Thuan ^{[6
]}

Na, MinKyun ^{[2
]}

机构：

[1] Natl Inst Med Mat, Hanoi, Vietnam

[2] Chungnam Natl Univ, Coll Pharm, Taejon 305764, South Korea

[3] Chonnam Natl Univ, Coll Pharm, Kwangju 500757, South Korea

[4] Univ Mississippi, Sch Pharm, Dept Pharmacognosy, University, MS 38677 USA

[5] Univ Mississippi, Sch Pharm, Pharmaceut Sci Res Inst, University, MS 38677 USA

[6] Vietnam Acad Tradit Med, Hanoi, Vietnam

来源：

PHYTOTHERAPY RESEARCH | 2014年 / 28卷 / 02期

基金：

新加坡国家研究基金会;

关键词：

Paeonia suffruticosa; palbinone; heme oxygenase-1; Nrf2; activation; PI3K; Akt pathways; ERK1; 2; pathways; NRF2 TRANSCRIPTION FACTOR; PHOSPHATIDYLINOSITOL; 3-KINASE/AKT; EXPRESSION; PATHWAYS;

D O I：

10.1002/ptr.4993

中图分类号：

R914 [药物化学];

学科分类号：

100701 ;

摘要：

Paeonia suffruticosa has been traditionally employed for vitalizing blood circulation and alleviating liver and inflammatory diseases. The pathways by which palbinone (PB) isolated from P. suffruticosa mediates heme oxygenase-1 (HO-1) induction were investigated using the specific inhibitors for PI3K and mitogen activated protein kinases pathways. The effect of PB-treatment on Nrf2 translocalization and HO-1-antioxidant response element (ARE) regulation was examined employing Western blot and luciferase assays. PB induced HO-1 expression via the activation of Nrf2 in the hepatic cells, and ARE-dependent genes were stimulated via the PB-mediated Nrf2 activation. PB-mediated HO-1 expression could be involved with PI3K/Akt and ERK1/2 pathways. Our study suggests the mechanism by which PB induces HO-1 expression in the hepatic cells. This might substantiate the traditional applications of P. suffruticosa for the treatment of oxidative stress-related diseases including oxidant and inflammatory-mediated vascular and liver diseases. Copyright (c) 2013 John Wiley & Sons, Ltd.

引用

页码：308 / 311

页数：4

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