Abstract
We investigated the potential ability of quercetin to protect against lipopolysaccharide (LPS)-induced intestinal oxidative stress in broiler chickens and the potential role of the Nrf2 (nuclear factor erythroid 2-related factor 2) signaling pathway. One-day-old broiler chickens (n = 240) were randomized into four groups: saline-challenged broiler chickens fed a basal diet (Con), LPS-challenged broiler chickens on a basal diet (LPS), and LPS-treated broiler chickens on a basal diet containing either 200 or 500 mg/kg of quercetin (Que200+LPS or Que500+LPS). Quercetin (200 mg/kg) significantly alleviated LPS-induced decreased duodenal, jejunal, and illeal villus height and increased the crypt depth in these regions. Quercetin significantly inhibited LPS-induced jejunal oxidative stress, including downregulated reactive oxygen species (ROS), malondialdehyde (MDA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, and it upregulated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. Quercetin relieved LPS-induced jejunal mitochondria damage and upregulated mitochondrial DNA copy number-related gene expression, including cytochrome c oxidase subunit 1 (COX1), ATP synthase F0 subunit 6 (ATP6), and NADH dehydrogenase subunit 1 (ND1). Quercetin attenuated the LPS-induced inhibition of Nrf2 activation, translocation, and downstream gene expression, including heme oxygenase-1 (HO-1), NAD (P) H dehydrogenase quinone 1 (NQO1), and manganese superoxide dismutase (SOD2). Additionally, quercetin attenuated the LPS-inhibition of c-Jun N-terminal kinase (JNK), Extracellular Regulated protein Kinases (ERK), and p38MAPK (p38) phosphorylation in the MAPK pathway. Thus, quercetin attenuated LPS-induced oxidative stress in the intestines of broiler chickens via the MAPK/Nrf2 signaling pathway.
Highlights
Bacterial infection is a major cause of intestinal oxidative stress [1]
LPS injection significantly decreased the ratio of villus height to crypt depth (VCR) (p < 0.05)
LPS significantly reduced the phosphorylation levels of Extracellular Regulated protein Kinases (ERK), Jun N-terminal kinase (JNK), and p38, while these reductions (p < 0.05; Figure 4). These results indicated that quercetin could increase the quercetin alleviated these reductions (p < 0.05; Figure 4). These results indicated that quercetin could phosphorylation/activation of ERK, JNK, and p38
Summary
Bacterial infection is a major cause of intestinal oxidative stress [1]. Bacterial infections seriously affect intestinal health and growth performance [2]. Lipopolysaccharide (LPS), a Gram-negative bacteria cell wall component, is an effective biostimulant for the immune system. LPS could induce reactive oxygen species (ROS) production and damage to lipids, producing a biomarker of lipid degradation (malondialdehyde, MDA) [3,4,5]. LPS could regulate intestinal oxidative status, leading to intestinal injury in broiler chickens [6]. Antibiotics have been widely used in the broiler industry, which has caused more prominent problems, such as bacterial resistance [7]. It is very important to replace antibiotics with an effective feed additive that can protect broiler chickens from intestinal oxidative stress
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