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Nutrients 2016, 8(10), 656; doi:10.3390/nu8100656

Proanthocyanidins Attenuation of Chronic Lead-Induced Liver Oxidative Damage in Kunming Mice via the Nrf2/ARE Pathway

1,2,†
,
3,†
,
1,2
,
1,2
,
1,2
and
1,*
1
Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China
2
College of Life Engineering, Shenyang Institute of Technology, Fushun 113122, China
3
School of Chemical Engineering, Sichuan University of Science and Engineering, Zigong 643000, China
These authors contributed equally to this study.
*
Author to whom correspondence should be addressed.
Received: 29 August 2016 / Revised: 5 October 2016 / Accepted: 14 October 2016 / Published: 21 October 2016
(This article belongs to the Special Issue Antioxidants in Health and Disease)
View Full-Text   |   Download PDF [4141 KB, uploaded 21 October 2016]   |  

Abstract

Lead is harmful for human health and animals. Proanthocyanidins (PCs), a natural antioxidant, possess a broad spectrum of pharmacological and medicinal properties. However, its protective effects against lead-induced liver damage have not been clarified. This study was aimed to evaluate the protective effect of PCs on the hepatotoxicity of male Kunming mice induced by chronic lead exposure. A total of 70 healthy male Kunming mice were averagely divided into four groups: control group, i.e., the group exposed to lead, the group treated with PCs, and the group co-treated with lead and PCs. The mice exposed to lead were given water containing 0.2% lead acetate. Mice treated in the PCs and PCs lead co-treated groups were given PC (100 mg/kg) in 0.9% saline by oral gavage. Lead exposure caused a significant elevation in the liver function parameters, lead level, lipid peroxidation, and inhibition of antioxidant enzyme activities. The induction of oxidative stress and histological alterations in the liver were minimized by co-treatment with PCs. Meanwhile, the number of Transferase-Mediated Deoxyuridine Triphosphate-Biotin Nick End Labeling (TUNEL)-positive cells was significantly reduced in the PCs/lead co-treated group compared to the lead group. In addition, the lead group showed an increase in the expression level of Bax, while the expression of Bcl-2 was decreased. Furthermore, the lead group showed an increase in the expression level of endoplasmic reticulum (ER) stress-related genes and protein (GRP78 and CHOP). Co-treated with PCs significantly reversed these expressions in the liver. PCs were, therefore, demonstrated to have protective, antioxidant, and anti-ER stress and anti-apoptotic activities in liver damage caused by chronic lead exposure in the Kunming mouse. This may be due to the ability of PCs to enhance the ability of liver tissue to protect against oxidative stress via the Nrf2/ARE signaling pathway, resulting in decreasing ER stress and apoptosis of liver tissue. View Full-Text
Keywords: proanthocyanidin; lead; oxidative damage; Nrf2/ARE pathway; liver; mice; apoptosis; ER stress proanthocyanidin; lead; oxidative damage; Nrf2/ARE pathway; liver; mice; apoptosis; ER stress
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Long, M.; Liu, Y.; Cao, Y.; Wang, N.; Dang, M.; He, J. Proanthocyanidins Attenuation of Chronic Lead-Induced Liver Oxidative Damage in Kunming Mice via the Nrf2/ARE Pathway. Nutrients 2016, 8, 656.

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