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.

The aim of this study was to investigate the effects of quercetin on inflammatory response and intestinal microflora in broiler chicken jejuna. A total of 120 broiler chickens were allocated into 3 groups: saline-challenged broilers fed a basal diet (CTR group), lipopolysaccharide (LPS)-challenged broilers fed a basal diet (L group) and LPS-challenged broilers fed a basal diet supplemented with 200 mg/kg quercetin (LQ group). Our results showed that LPS significantly increased expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8, interferon (IFN)-γ, toll-like receptor (TLR)-4, Bax, Caspase-3 and diamine oxidase activity (DAO), and decreased expression of zona occludens-1 (ZO-1), Occludin and Bcl-2 in the jejunum, while dietary quercetin prevented the adverse effects of LPS injection. LPS injection significantly decreased the number of Actinobacteria, Armatimonadetes and Fibrobacteriae at the phylum level when compared to the CTR group. Additionally, at genus level, compared with the CTR group, the abundance of Halomonas, Micromonospora, Nitriliruptor, Peptococcus, Rubellimicrobium, Rubrobacter and Slaclda in L group was significantly decreased, while dietary quercetin restored the numbers of these bacteria. In conclusion, our results demonstrated that dietary quercetin could alleviate inflammatory responses of broiler chickens accompanied by modulating jejunum microflora.

High copper feed has been widely used as an inexpensive and highly effective feed additive to promote growth performance of pigs. However, long‐term feeding of high copper feed may reduce the growth‐promoting effects of copper, time‐dependent accumulation of copper in animal tissues and organs, and copper toxicity thereby reducing the growth performance of pigs. Due to the widespread effects of high copper supplementation in animals' diets, the benefits and drawbacks of high copper feeding in pigs have been reported in several studies. Meanwhile, few of these studies have systematically described the mechanism by which high copper diets restrain pig growth. Therefore, to address the concerns and give a better understanding of the mechanism of high copper diet in restraining pig growth in different systems, this paper reviews the research progress of long‐term supplementation of high copper on the growth of pigs and provides some suggestions and further research directions.

The 17β-estradiol (E2)-degrading bacterium Rhodococcus sp.RCBS9 previously showed remarkable resistance to the combined stresses of low temperature and E2. In this study, physiological experiments and transcriptomic analysis were performed to investigate the mechanisms underlying the strain's low-temperature adaptation and briefly analyze how it maintains its ability to degrade E2 at low temperature. The results showed that the strain's signal transduction functions, adaptive changes in cell membrane and cell wall structure, gene repair functions, and synthesis of antioxidants and compatible solutes are key to its ability to adapt to low temperature. In addition, its stress proteins in response to low temperature were not typical cold shock proteins, but rather universal stress proteins (USPs) and heat shock proteins (HSPs), among others. The strain also upregulated biofilm production, transporter proteins for carbon source uptake, and proteins for fatty acid degradation to ensure energy generation. The strain's multiple stress responses work synergistically to resist low-temperature stress, ensuring its adaptability to low-temperature environments and ability to degrade E2. Finally, six genes related to survival at low temperature (identified in the transcriptome analysis) were expressed in E. coli BL21, and they were found to contribute to recombinant E. coli growth at low temperature.