Chlorogenic acid (CGA) is a bioactive substance with anti-inflammatory activities. Clusters of CD36 have been suggested to be widely involved in inflammatory damage. However, the mechanism of CGA protecting against LPS-induced inflammation involving the CD36 regulation is unclear. Here, we demonstrated that CGA protected against LPS-induced cell death and decreased the production of ROS. Moreover, the SOD, CAT, and GSH-Px activities were also upregulated in CGA-treated cells during LPS stimulation. CGA reduced COX-2 and iNOS expression and IL-1β, IL-6, and TNF-α secretion in LPS-stimulated RAW264.7 macrophages. In addition, CGA treatment widely involved in immune-related signaling pathways, including NF-κB signaling, NOD-like receptor signaling, and IL-17 signaling using transcriptomic analysis and CD36 also markedly reduced during CGA pretreatment in LPS-induced RAW264.7 cells. Furthermore, the CD36 inhibitor SSO attenuated inflammation and oxidative stress by enabling activation of the AMPK/PGC-1α cascade. These results indicate that CGA might provide benefits for the regulation of inflammatory diseases by modulating CD36/AMPK/PGC-1α to alleviate oxidative stress.

Background: Cage-rearing in laying ducks, as a novel rearing system, not only fundamentally solves the pollution problem of the duck industry and improve bio-safety and product quality but also exhibits more benefits by implementing standardized production compared with the floor-rearing. Of course, this system also brings some welfare problems and stress injuries to layers due to lack of water environment and limited activities in the cages. However, the effects on the factors of antioxidant defense and inflammatory injury in the early cage stage are not well-understood. Results: In this study, eighty Shaoxing layers were reared on floor and in cages from 12 weeks of age. The ducks were caged 1, 2, 4, 7, and 10 days, the factors of antioxidant defense and inflammatory injury were investigated. The results showed that the caged ducks suffered liver injury to a certain extent when the ducks were just put into the cages. Analysis of antioxidant enzyme activities indicated that the different rearing system could not affect the change of antioxidant capacities, while the liver malondialdehyde (MDA) level was significant higher in the 2-d, 7-d, and 10-d ducks compared with the 1-d ducks during the change of days, while catalase (CAT) activity showed the opposite results. Additionally, quantitative real-time PCR (qRT-RCR) revealed that the relative mRNA levels of endoplasmic reticulum (ER) stress-related gene (CHOP and GRP78) were significantly upregulated in cage rearing ducks compared to that of the floor rearing ducks. Moreover, the mRNA levels of inflammatory cytokines including cycloxygenase-2 (COX-2), nitric oxide synthase (iNOS), Interleukin 1 beta (IL-1β), Interleukin 2 (IL-2) and Interleukin 6 (IL-6), were also increased significantly in caged layers. Conclusions: Taken together, although antioxidant defense has no obvious effect on cage stress, the stress levels of laying ducks vary greatly in the early cage stage, which not only caused liver tissue damage to some extent, but also resulted in increases in the expression of the factors of inflammatory injury. Therefore, we recommend that anti-stress agents should be added in the feed to alleviate the stress in the early cage stage.

NOD-like receptors (NLRs) are a family of cytoplasmic pattern recognition receptors (PRRs), of which NOD1 and NOD2, are the main representative members. Many investigations have focused on the role of NOD1 and NOD2 in the innate immune response in Cypriniformes and Siluriformes. As an important economic fish in Perciformes, little is known about the function of NOD1 and NOD2 in mandarinfish (Siniperca chuatsi). The full-length NOD1 and NOD2 cDNA sequence was obtained using reverse transcription polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends (RACE). The mandarinfish NOD1 and NOD2 cDNA sequences contain 3247 bp and 3257 bp, and encode 918 amino acids and 988 amino acids, respectively. Multiple sequence alignments showed that mNOD1 and mNOD2 share high similarity with that from other vertebrates. RT-PCR analysis revealed that relatively high levels of mNOD1 and mNOD2 mRNA were detected in gill and head kidney tissues, compared with the heart, spleen, liver, muscle, and intestine. In addition, the relative levels of mNOD1 and mNOD2 transcripts were significantly upregulated in three tissues when the fishes were challenged with LPS and Poly I:C, interestingly, the NOD1 mRNA got peaked earlier than NOD2 after LPS induction in the spleen, gill, and head kidney, and during Poly I:C treatment, the NOD2 mRNA got peaked at 8 h in spleen and gill, while NOD1 showed significant higher expression at 24 h post infection, besides, in head kidney, the NOD2 mRNA showed a great increasing trend and NOD1 got peaked at 16 h. Therefore the mNOD1 and mNOD2 may act differently within different tissues in different time during antiviral and antibacterial defense. These results revealed the dynamic mNOD1 and mNOD2 expression during viral and bacterial infections, which suggested the NOD1 and NOD2 play important roles in innate immune of mandarinfish.

Broodiness is an unfavorable trait associated with the cessation of egg laying. Studies have found that excessive granulosa cell apoptosis and autophagy occur during goose broodiness. Other studies have also confirmed that oxidative stress is an important cause of apoptosis and autophagy. However, whether oxidative stress occurs during goose broodiness and whether this oxidative stress causes apoptosis and autophagy have not been fully elucidated. In this study, we investigated the effects of oxidative stress on the autophagy and apoptosis of granulosa cells in broody geese. The results showed higher mRNA expression of genes related to antioxidative stress responses (GPX, SOD-1, SOD-2, COX-2, CAT and hsp70) in pre-broody and broody geese than in laying birds. In addition, increased levels of granulosa cell apoptosis and autophagy were observed in pre-broody geese than in laying geese. Additionally, granulosa cells treated with H₂O₂ exhibited increased apoptosis and autophagy in vitro, and these effects were responsible for goose granulosa cell death. Moreover, vitamin E treatment effectively protected granulosa cells from H₂O₂-induced oxidative stress by inhibiting ROS production. Correspondingly, granulosa cell apoptosis and autophagy were greatly alleviated by vitamin E treatment. Together, our results demonstrated serious oxidative stress and granulosa cell apoptosis and autophagy in broody geese, and oxidative stress promoted apoptosis and autophagy. Vitamin E alleviated the autophagy and apoptosis of granulosa cells by inhibiting oxidative stress.

Microplastics (MPs) are widespread environmental pollutants that can enter the human body through the food chain, potentially leading to lung damage. However, the underlying mechanisms responsible for this damage remain unclear. Ducks, a commonly consumed poultry species in China, are particularly susceptible to MPs exposure due to their farming environment. In this study, Shaoxing ducklings were administered two distinct concentrations of polystyrene microplastics (PS-MPs) (1 mg/L and 100 mg/L) via oral route, alongside a control group, over a period of four weeks to establish an in vivo model for evaluating the effects of microplastic exposure in ducks. Simultaneously, rat type II alveolar epithelial (RLE-6TN) cells were exposed to different concentrations of PS-MPs (0, 10, 100, and 500 µg/mL) for 48 h, thereby constructing an in vitro exposure model. Our results showed that PS-MPs caused pathological damage, inflammatory cell infiltration, and activation of the LPS/TLR4 inflammatory pathway in the lung. Further analysis revealed that PS-MPs disrupted the tricarboxylic acid (TCA) cycle and inhibited oxidative phosphorylation. Mechanistic investigation demonstrated that PS-MPs induced mitochondrial dysfunction and consequent excessive mitophagy. This study investigates the mechanisms by which PS-MPs contribute to mitochondrial dysfunction and mitophagy, potentially exacerbating lung inflammation, offering valuable insights for mitigating the toxic effects of PS-MPs on human and animal health.

The objective of this study was to investigate the effects of tributyrin supplementation on liver fat metabolism in broiler chickens. Two hundred and forty broilers were randomly allocated into two experimental groups (6 replicates per treatment; 20 chickens in each replicate): the control group (CN), which received a basal diet, and the tributyrin group (TB), which received a basal diet supplemented with 1 g/kg of tributyrin. The experimental period lasted 37 days. The results showed that in the liver, broilers supplemented with tributyrin had higher content of high-density lipoprotein cholesterol (HDL-C) (p < 0.05). Liver hepatic lipase (HL), lipoprotein lipase (LPL) and total lipid (TL) activity were significantly lower than in the TB group than that in the NC group. Meanwhile, the diet supplemented with tributyrin had more lipid droplets than the NC group, whereas the TB and NC groups showed no histological abnormalities in the liver. Furthermore, the mRNA expression levels of peroxisome proliferators-activated receptor α (PPARα), proliferators-activated receptor γ (PPARγ), fatty acid synthase (FAS), LPL and adipose triglyceride lipase (ATGL) in the liver were significantly upregulated in the TB group (p < 0.05), while those of the long-chain acyl-CoA-synthetase 1 (ACSL1) mRNA between the TB group and the NC group were not different (p > 0.05). These findings indicated that the diet supplemented with tributyrin could increase fat deposition appropriately by promoting fat synthesis without causing liver tissue damage, which demonstrated that tributyrin can be considered a valid feed additive for broiler chickens.