This study investigates the effects of quercetagetin (QG) supplementation on the antioxidant capacity, liver mitochondrial function, and cecal microbiota of broilers raised under high-density conditions. A 2 × 2 factorial design with 144 one-day-old WOD168 broilers, which were allocated to two stocking densities (LD: 4 birds per cage, equivalent to 11.1 birds per square meter; HD: eight birds per cage, equivalent to 22.2 birds per square meter) and two levels of dietary supplementation of QG (0 and 20 mg/kg). At the conclusion of day 21, broilers of similar body weights were randomly allocated into four groups (22 to 42 d): control (CON), QG treatment (QG), high stocking density (HSD), and high stocking density with QG supplementation (H_QG). The results demonstrated that HD groups significantly reduced broiler growth performance, including body weight (BW), average daily gain (ADG), and average daily feed intake (ADFI) ( < 0.05). Additionally, HD groups increased serum stress hormone levels (CORT and ACTH), pro-inflammatory cytokines (IL-1β and IL-6) ( < 0.05), while decreasing liver antioxidant enzyme activities (GSH-Px, T-SOD), serum CAT and T-SOD activities, and mitochondrial function (GSH, complex I-III, ATP contents) ( < 0.05). However, dietary supplementation with 20 mg/kg QG significantly alleviated the negative effects induced by HSD, restoring growth performance, stress hormone levels, immune parameters, and liver antioxidant and mitochondrial function. Moreover, QG supplementation markedly improved cecal microbiota composition, enhancing gut health. Correlation analysis revealed a strong association between microbial composition and overall broiler health, indicating that gut microbiota plays a critical role in mediating these beneficial effects. In conclusion, QG exhibits protective effects against oxidative stress, mitochondrial dysfunction, and gut microbiota imbalance induced by high-density rearing, suggesting its potential as a functional feed additive to improve broiler health under intensive farming conditions.
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http://dx.doi.org/10.3390/ani15030398 | DOI Listing |
J Immunol
January 2025
Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, P. R. China.
The von Hippel-Lindau (VHL) tumor suppressor gene VHL is a classic tumor suppressor that has been identified in family members with clear cell renal cell carcinomas, central nervous system and retinal hemangioblastomas, phaeochromocytomas, and pancreatic neuroendocrine tumors. The well-defined function of VHL is to mediate proteasomal degradation of hydroxylated hypoxia-inducible factor α proteins, resulting in the downregulation of hypoxia-responsive gene expression. Previously, we reported that VHL inhibits antiviral signaling by targeting mitochondrial antiviral signaling protein (MAVS) for proteasomal degradation.
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January 2025
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA, United States.
Macrophages are critical to maintaining and restoring tissue homeostasis during inflammation. The lipid metabolic state of macrophages influences their function and polarization, which is crucial to the resolution of inflammation. The contribution of lipid synthesis to proinflammatory macrophage responses is well understood.
View Article and Find Full Text PDFJ Immunol
February 2025
Department of Pharmacology and Toxicology, University of Arizona, Tucson, AZ, United States.
Mitochondrial antiviral-signaling protein (MAVS) is a key adapter protein required for inducing type I interferons (IFN-Is) and other antiviral effector molecules. The formation of MAVS aggregates on mitochondria is essential for its activation; however, the regulatory mitochondrial factor that mediates the aggregation process is unknown. Our recent work has identified the protein Aggregatin as a critical seeding factor for β-amyloid peptide aggregation.
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March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFSci Adv
March 2025
Department of Radiation Oncology, Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Lung cancer exhibits altered metabolism, influencing its response to radiation. To investigate the metabolic regulation of radiation response, we conducted a comprehensive, metabolic-wide CRISPR-Cas9 loss-of-function screen using radiation as selection pressure in human non-small cell lung cancer. Lipoylation emerged as a key metabolic target for radiosensitization, with lipoyltransferase 1 (LIPT1) identified as a top hit.
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