Dietary Supplementation of Blueberry Juice Enhances Hepatic Expression of Metallothionein and Attenuates Liver Fibrosis in Rats
Identifieur interne : 002617 ( Ncbi/Curation ); précédent : 002616; suivant : 002618Dietary Supplementation of Blueberry Juice Enhances Hepatic Expression of Metallothionein and Attenuates Liver Fibrosis in Rats
Auteurs : Yuping Wang [République populaire de Chine] ; Mingliang Cheng [République populaire de Chine] ; Baofang Zhang [République populaire de Chine] ; Fei Nie [République populaire de Chine] ; Hongmei Jiang [République populaire de Chine]Source :
- PLoS ONE [ 1932-6203 ] ; 2013.
Abstract
To investigate the effect of blueberry juice intake on rat liver fibrosis and its influence on hepatic antioxidant defense.
Rabbiteye blueberry was used to prepare fresh juice to feed rats by daily gastric gavage. Dan-shao-hua-xian capsule (DSHX) was used as a positive control for liver fibrosis protection. Liver fibrosis was induced in male Sprague-Dawley rats by subcutaneous injection of CCl4 and feeding a high-lipid/low-protein diet for 8 weeks. Hepatic fibrosis was evaluated by Masson staining. The expression of α-smooth muscle actin (α-SMA) and collagen III (Col III) were determined by immunohistochemical techniques. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in liver homogenates were determined. Metallothionein (MT) expression was detected by real-time RT-PCR and immunohistochemical techniques.
Blueberry juice consumption significantly attenuates CCl4-induced rat hepatic fibrosis, which was associated with elevated expression of metallothionein (MT), increased SOD activity, reduced oxidative stress, and decreased levels of α-SMA and Col III in the liver.
Our study suggests that dietary supplementation of blueberry juice can augment antioxidative capability of the liver presumably via stimulating MT expression and SOD activity, which in turn promotes HSC inactivation and thus decreases extracellular matrix collagen accumulation in the liver, and thereby alleviating hepatic fibrosis.
Url:
DOI: 10.1371/journal.pone.0058659
PubMed: 23554912
PubMed Central: 3595269
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<author><name sortKey="Wang, Yuping" sort="Wang, Yuping" uniqKey="Wang Y" first="Yuping" last="Wang">Yuping Wang</name>
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<author><name sortKey="Cheng, Mingliang" sort="Cheng, Mingliang" uniqKey="Cheng M" first="Mingliang" last="Cheng">Mingliang Cheng</name>
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<author><name sortKey="Zhang, Baofang" sort="Zhang, Baofang" uniqKey="Zhang B" first="Baofang" last="Zhang">Baofang Zhang</name>
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<author><name sortKey="Jiang, Hongmei" sort="Jiang, Hongmei" uniqKey="Jiang H" first="Hongmei" last="Jiang">Hongmei Jiang</name>
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<front><div type="abstract" xml:lang="en"><sec><title>Aim</title>
<p>To investigate the effect of blueberry juice intake on rat liver fibrosis and its influence on hepatic antioxidant defense.</p>
</sec>
<sec><title>Methods</title>
<p>Rabbiteye blueberry was used to prepare fresh juice to feed rats by daily gastric gavage. Dan-shao-hua-xian capsule (DSHX) was used as a positive control for liver fibrosis protection. Liver fibrosis was induced in male Sprague-Dawley rats by subcutaneous injection of CCl<sub>4</sub>
and feeding a high-lipid/low-protein diet for 8 weeks. Hepatic fibrosis was evaluated by Masson staining. The expression of α-smooth muscle actin (α-SMA) and collagen III (Col III) were determined by immunohistochemical techniques. The activities of superoxide dismutase (SOD) and malondialdehyde (MDA) in liver homogenates were determined. Metallothionein (MT) expression was detected by real-time RT-PCR and immunohistochemical techniques.</p>
</sec>
<sec><title>Results</title>
<p>Blueberry juice consumption significantly attenuates CCl<sub>4</sub>
-induced rat hepatic fibrosis, which was associated with elevated expression of metallothionein (MT), increased SOD activity, reduced oxidative stress, and decreased levels of α-SMA and Col III in the liver.</p>
</sec>
<sec><title>Conclusion</title>
<p>Our study suggests that dietary supplementation of blueberry juice can augment antioxidative capability of the liver presumably via stimulating MT expression and SOD activity, which in turn promotes HSC inactivation and thus decreases extracellular matrix collagen accumulation in the liver, and thereby alleviating hepatic fibrosis.</p>
</sec>
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<author><name sortKey="Carrere, N" uniqKey="Carrere N">N Carrere</name>
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