Dietary resveratrol improves antioxidant status of sows and piglets and regulates antioxidant gene expression in placenta by Keap1-Nrf2 pathway and Sirt1

Qingwei Meng,Baoming Shi,Anshan Shan,Shiqi He,Tao Guo,Gaoqiang Li,Baojing Cheng,Shishuai Sun

doi:10.1186/s40104-018-0248-y

Abstract

BackgroundResveratrol, a plant phenol, affords protection against inflammation and oxidative stress. The objective of this study was to investigate the effects of dietary resveratrol supplementation during pregnancy and lactation on the antioxidant status of sows and piglets and on antioxidant gene expression and pathway in placenta.MethodsForty sows were allotted to 2 dietary treatments 20 d after breeding. Sows were fed a control diet and a control diet with 300 mg/kg resveratrol. Oxidative stress biomarkers and antioxidant enzymes were measured in the placenta, milk, and plasma of sows and piglets. Antioxidant gene expression and protein expression of Kelch-like ECH-associated protein 1-Nuclear factor E2-related factor 2 (Keap1-Nrf2), nuclear factor kappa B-p65 (NFκB-p65) and sirtuin1 (Sirt1) were quantified in the placenta.ResultsDietary resveratrol increased the litter and piglets weaning weights. Antioxidant status in the milk, placenta and plasma of sows and piglets was partially improved by dietary resveratrol. In placenta, Nrf2 protein expression was increased and Keap1 protein expression was decreased by dietary resveratrol. The mRNA expression of antioxidant genes including catalase (CAT), glutathione peroxidase 1 (GPX1), GPX4, superoxide dismutase 1 (SOD1) and heme oxygenase 1 (HO1), and phase 2 detoxification genes, including glutamate-cysteine ligase modifier (GCLM), microsomal glutathione S-transferase 1(MGST1) and UDP glucuronosyltransferase family 1 member A1 (UGT1A1), was increased by dietary resveratrol. Dietary resveratrol also increased Sirt1 and phosphorylated NFκB-p65 protein expression in the placenta. We failed to observe any influences of dietary resveratrol on pro-inflammatory cytokine levels, including those of interleukin 1β (IL-1β), IL-6, IL-8 and tumor necrosis factor α (TNF-α). However, we observed that the mRNA expression of IL-8 in placenta was reduced by maternal resveratrol. In addition, dietary resveratrol showed interactive effects with day of lactation on activities of SOD and CAT and levels of malonaldehyde (MDA) and hydrogen peroxide (H2O2) in milk.ConclusionsDietary resveratrol supplementation during pregnancy and lactation improves the antioxidant status of sows and piglets, which is beneficial to the reproductive performance of sows. Dietary resveratrol regulates placental antioxidant gene expression by the Keap1-Nrf2 pathway and Sirt1 in placenta.

Highlights

Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress
Dietary resveratrol supplementation in gestation and lactation diets had no effects on back-fat thickness gain during gestation or loss during lactation (P > 0.05)
Pre-weaning survival rate was not affected by dietary resveratrol supplementation during gestation or lactation (P > 0.05)

Summary

Introduction

Resveratrol, a plant phenol, affords protection against inflammation and oxidative stress. An imbalance between pro-oxidative and anti-oxidative forces in biological systems, may cause both lipid and protein oxidation and impair normal cell function. This imbalance is considered to be responsible for the initiation or development of pathological processes affecting female reproductive processes [1, 2]. Studies have confirmed that sows suffer elevated and systemic oxidative stress during late gestation and lactation [4, 5]. Tan et al [5] reported that sows suffered increased oxidative stress during delivery, late gestation and early lactation, as indicated by their elevated ROS, 8-hydroxydeoxyguanosine, and thiobarbituric acid reactive substance levels. Oxidative stress has been suggested as a causative agent in human and animal pregnancy-related disorders, such as embryonic reabsorption, recurrent pregnancy loss, preeclampsia, intra-uterine growth restriction and fetal death, which are predictive of an elevated risk of the metabolic syndrome in postnatal life and may be a common pathway in developmental metabolic programming [7, 8]

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