Dairy farming is the most important economic activity in animal husbandry. Mastitis is the most common disease in dairy cattle and has a significant impact on milk quality and yield. The natural extract allicin, which is the main active ingredient of the sulfur-containing organic compounds in garlic, has anti-inflammatory, anticancer, antioxidant, and antibacterial properties; however, the specific mechanism underlying its effect on mastitis in dairy cows needs to be determined. Therefore, in this study, whether allicin can reduce lipopolysaccharide (LPS)-induced inflammation in the mammary epithelium of dairy cows was investigated. A cellular model of mammary inflammation was established by pretreating bovine mammary epithelial cells (MAC-T) with 10 µg/mL LPS, and the cultures were then treated with varying concentrations of allicin (0, 1, 2.5, 5, and 7.5 µM) added to the culture medium. MAC-T cells were examined using RT–qPCR and Western blotting to determine the effect of allicin. Subsequently, the level of phosphorylated nuclear factor kappa-B (NF-κB) was measured to further explore the mechanism underlying the effect of allicin on bovine mammary epithelial cell inflammation. Treatment with 2.5 µM allicin considerably decreased the LPS-induced increase in the levels of the inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) and inhibited activation of the NOD-like receptor protein 3 (NLRP3) inflammasome in cow mammary epithelial cells. Further research revealed that allicin also inhibited the phosphorylation of inhibitors of nuclear factor kappa-B-α (IκB-α) and NF-κB p65. In mice, LPS-induced mastitis was also ameliorated by allicin. Therefore, we hypothesize that allicin alleviated LPS-induced inflammation in the mammary epithelial cells of cows probably by affecting the TLR4/NF-κB signaling pathway. Allicin will likely become an alternative to antibiotics for the treatment of mastitis in cows.
This study aimed to investigate the effect of summer and winter on slaughter performance, muscle quality, flavor-related substance content, and gene expression levels related to the fat metabolism of pheasants. One-hundred 1-day-old pheasants were fed for 5 months starting in March and July and then, respectively, slaughtered in summer (August) and winter (December). The results revealed that compared with summer, winter not only increased pheasant live weight, dressed percentage, fulleviscerated yield, and muscle yield (p < 0.05) but also enhanced the activities of SOD and CAT in serum (p < 0.05). Winter significantly increased meat color, the contents of inosinic acid, and flavor amino acid in muscle. Amino acid contents in leg muscles of pheasants in winter were significantly higher than in summer except for histidine (p < 0.05). Winter increased the contents of muscle mono-unsaturated fatty acid, reducing saturated fatty acid. Summer improved fat synthesis in liver, promoted the deposition of triglycerides and cholesterol, and reduced the expression levels of fat metabolism-related genes in muscle, while winter increased the expression levels of genes related to muscle fat metabolism to provide energy for body and affect muscle fatty acid profile. Overall, pheasants fed in winter had better sensory quality and flavor than summer.
Although there has been enormous progress in the last half-century in the drug discovery targeting obesity and associated co-morbidities, the clinical treatment of obesity remains tremendously challenging. GPR75 is an orphan receptor and is suggested to be a potential novel target for the control of obesity and related metabolic disorders. Inhibition of the GPR75 signaling pathway by small molecules, antibodies, or genetic manipulations may provide a therapeutic strategy for obesity. Here, we report the active-like Cryo-EM structure of human GPR75 with an intracellular nanobody, which reveals the receptor activation mechanism. The extensive interaction network required to achieve the active structure helps explain the allosteric coupling between the orthosteric pocket and the G-protein coupling domain. The well-defined orthosteric ligand binding pocket of human GPR75 provides a structural basis for anti-obesity drug discovery.
Objective: Bacteria-induced mastitis is characterized by mammary pain, swelling of the mammary glands, and decreased milk production and quality in cows. Reducing the negative effects of inflammation is a challenge, and the regulatory mechanism of the inflammatory response in mammary epithelial cells is not yet clear. Results: Our results indicated that the RNA-binding protein Musashi2 (Msi2) regulates the inflammatory response and the blood-milk barrier in mastitis. Msi2 is commonly enriched in stem cells and tumor cells. We found that Msi2 expression was upregulated during mastitis. Silencing Msi2 in BMECs and mice increased inflammatory factors and tight junctions. Transcriptional profiling analysis revealed that Msi2 silencing increased transforming growth factor-beta (TGFβ) signaling. RNA-interacting protein immunoprecipitation assays demonstrated that Msi2 could affect the translation of transforming growth factor-beta receptor 1 (TGFβR1), thereby affecting TGFβ signaling. Overall, Msi2 silencing reduced inflammatory reactions and repaired the blood-milk barrier during mastitis Conclusions: Our findings indicate that Msi2 plays an important role in mastitis by regulating the TGFβ signaling pathway. A decrease in Msi2 can reduce the negative effects of mastitis by inhibiting the expression of inflammatory factors and increasing tight junction proteins.
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