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CLC number: R96

On-line Access: 2014-12-03

Received: 2014-04-14

Revision Accepted: 2014-07-20

Crosschecked: 2014-11-14

Cited: 14

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Citations:  Bibtex RefMan EndNote GB/T7714


Li-li JI


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Journal of Zhejiang University SCIENCE B 2014 Vol.15 No.12 P.1039-1047


Therapeutic detoxification of quercetin against carbon tetrachloide-induced acute liver injury in mice and its mechanism*

Author(s):  Jia-qi Zhang1,2, Liang Shi1,2, Xi-ning Xu2, Si-chong Huang2, Bin Lu1, Li-li Ji1, Zheng-tao Wang1

Affiliation(s):  1. MOE Key Laboratory for Standardization of Chinese Medicines and Shanghai Key Laboratory of Complex Prescription, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; more

Corresponding email(s):   lichenyue1307@126.com

Key Words:  Hepatotoxicity, Oxidative stress, Peroxiredoxin (Prx), Nuclear factor erythroid 2-related factor 2 (Nrf2), TrxR, Trx, HO-1

Jia-qi Zhang, Liang Shi, Xi-ning Xu, Si-chong Huang, Bin Lu, Li-li Ji, Zheng-tao Wang. Therapeutic detoxification of quercetin against carbon tetrachloride-induced acute liver injury in mice and its mechanism[J]. Journal of Zhejiang University Science B, 2014, 15(12): 1039-1047.

@article{title="Therapeutic detoxification of quercetin against carbon tetrachloride-induced acute liver injury in mice and its mechanism",
author="Jia-qi Zhang, Liang Shi, Xi-ning Xu, Si-chong Huang, Bin Lu, Li-li Ji, Zheng-tao Wang",
journal="Journal of Zhejiang University Science B",
publisher="Zhejiang University Press & Springer",

%0 Journal Article
%T Therapeutic detoxification of quercetin against carbon tetrachloride-induced acute liver injury in mice and its mechanism
%A Jia-qi Zhang
%A Liang Shi
%A Xi-ning Xu
%A Si-chong Huang
%A Bin Lu
%A Li-li Ji
%A Zheng-tao Wang
%J Journal of Zhejiang University SCIENCE B
%V 15
%N 12
%P 1039-1047
%@ 1673-1581
%D 2014
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1400104

T1 - Therapeutic detoxification of quercetin against carbon tetrachloride-induced acute liver injury in mice and its mechanism
A1 - Jia-qi Zhang
A1 - Liang Shi
A1 - Xi-ning Xu
A1 - Si-chong Huang
A1 - Bin Lu
A1 - Li-li Ji
A1 - Zheng-tao Wang
J0 - Journal of Zhejiang University Science B
VL - 15
IS - 12
SP - 1039
EP - 1047
%@ 1673-1581
Y1 - 2014
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1400104

This study observes the therapeutic detoxification of quercetin, a well-known flavonoid, against carbon tetrachloride (CCl4) induced acute liver injury in vivo and explores its mechanism. Quercetin decreased CCl4-increased serum activities of alanine and aspartate aminotransferases (ALT/AST) when orally taken 30 min after CCl4 intoxication. The results of a histological evaluation further evidenced the ability of quercetin to protect against CCl4-induced liver injury. Quercetin decreased the CCl4-increased malondialdehyde (MDA) and reduced the glutathione (GSH) amounts in the liver. It also reduced the enhanced immunohistochemical staining of the 4-hydroxynonenal (4-HNE) in the liver induced by CCl4. peroxiredoxin (Prx) 1, 2, 3, 5, 6, thioredoxin reductase 1 and 2 (trxR%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>trxR1/2), thioredoxin 1 and 2 (trx1/2), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) all play critical roles in maintaining cellular redox homeostasis. Real-time polymerase chain reaction (PCR) results demonstrated that quercetin reversed the decreased mRNA expression of all those genes induced by CCl4. In conclusion, our results demonstrate that quercetin ameliorates CCl4-induced acute liver injury in vivo via alleviating oxidative stress injuries when orally taken after CCl4 intoxication. This protection may be caused by the elevation of the antioxidant capacity induced by quercetin.


本研究旨在观察槲皮素对四氯化碳(CCl)诱导的肝损伤的治疗解毒作用及其机理。 首次发现槲皮素对CCl4诱导的肝损伤有治疗作用,并且首次发现Prx和Trx家族参与其中。 检测小鼠血清转氨酶含量,并检测肝组织中丙二醛(MDA)、谷胱甘肽(GSH)和4-羟基壬烯醛(4-HNE)含量,并用实时聚合酶链式反应(PCR)检测肝组织中Prx1-6、TrxR1/2、Trx1/2、Nrf2和HO-1的mRNA表达情况。 CCl4造模成功后口服槲皮素对其造成的急性肝损伤有治疗作用,给药组小鼠血清中的转氨酶与模型组相比均有显著下降,通过MDA和免疫组化分析其机理可能和保护氧化应激损伤有关,通过实时PCR分析发现CCl抑制了抗氧化酶Prx家族、TrxRd1、TrxRd2、Trx1、Trx2和Nrf2及其下游HO-1的基因表达,而槲皮素可以逆转CCl降低的这些基因的表达。

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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