Search

Objective To investigate the methylation status of the NOX5 gene in peripheral blood of patients with gestational diabetes mellitus (GDM) and its association with GDM. Methods A total of 67 pregnant women who were diagnosed with GDM at the outpatient service of Department of Obstetrics in our hospital from 2020 to 2021 were enrolled as case group, and 87 healthy pregnant women with normal oral glucose tolerance test results during the same period of time were enrolled as control group. Methylation-specific PCR was used to determine the methylation status of the NOX5 gene, and according to the methylation status of the NOX5 gene, the pregnant women in the case group were further divided into positive subgroup with 44 women and negative subgroup with 23 women. According to the presence or absence of fetal distress or fetal macrosomia, 154 neonates were divided into distress group with 6 neonates and non-distress group with 148 neonates, as well as fetal macrosomia group with 11 neonates and non-fetal macrosomia group with 143 neonates. The methylation status of the NOX5 gene was analyzed in terms of its association with the general information and pregnancy outcome of the pregnant women with GDM. Results There was a significant difference in the constituent ratio of positive NOX5 gene methylation between the case group and the control group (65.67% vs 40.23%,χ2=9.807,P0.05). There was no significant difference in the constituent ratio of positive NOX5 gene methylation between the distress group and the non-distress group and between the fetal macrosomia group and the non-fetal macrosomia group (P>0.05). Conclusion NOX5 gene methylation is often observed in pregnant women with GDM, but the methylation status of the NOX5 gene is not associated with the age, pre-pregnancy BMI, blood pressure, and fasting blood glucose of pregnant women with GDM, and it is also not associated with fetal distress and fetal macrosomia.

BACKGROUND: This study investigated the effects of dietary plant polysaccharides on growth performance, immune status and intestinal health in broilers. We randomly divided 960 one‐day‐old Arbor Acres broiler chicks into four groups. The control (CON) group was fed a basal diet, and the remaining groups were fed a basal diet supplemented with 1000 mg kg−1Ginseng polysaccharide (GPS), Astragalus polysaccharide (APS), or Salvia miltiorrhiza polysaccharide (SMP) for 42 days. RESULTS: Dietary supplementation with SMP significantly increased body weight (BW) at 21 and 42 days of age, average daily gain (ADG) and average daily feed intake (ADFI) during the starter and whole experimental period, decreased the concentrations of interleukin‐1 beta (IL‐1β), tumor necrosis factor α (TNF‐α) and malondialdehyde (MDA), increased the levels of interleukin‐4 (IL‐4) and interleukin‐10 (IL‐10) and catalase (CAT) activity in the serum (P < 0.05). GPS, APS, and SMP supplementation increased serum levels of immunoglobulins, activities of glutathione peroxidase (GSH‐Px), total superoxide dismutase (T‐SOD) and total antioxidant capacity (T‐AOC), and cecal concentrations of acetic acid and propionic acid of broilers (P < 0.05). Furthermore, high‐throughput sequencing results showed that the relative abundance of Firmicutes was decreased while the relative abundance of Bacteroidota, Alistipes, and Prevotellaceae_NK3B31_group were increased (P < 0.05) in the GPS, APS, and SMP groups compared with the CON group. CONCLUSION: Dietary GPS, APS, and SMP supplementation could improve growth performance, enhance immune function by increasing serum immunoglobulin and regulating cytokines, improve antioxidant function by increasing serum antioxidant enzyme activity, increase volatile fatty acid levels and improve the microbial composition in the cecum of broilers. Dietary SMP supplementation had the optimal effect in this study. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Simple Summary: The long-term overuse of zinc oxide by swine farms effectively alleviated the post-weaning diarrhea and improved the growth performance of piglets, whereas it also led to severe heavy metal residues and zinc emission pollution. Hence, finding traceable, safe, efficient and low-cost alternatives for zinc oxide is of great importance nowadays. In this study, sodium alginate-coated nano zinc oxide, a new type of zinc resource, was used and proved to be a potential alternative to traditional doses of zinc oxide, which showed beneficial effects on the growth performance, diarrhea rate, immune and antioxidant functions, zinc accumulation and excretion, short chain fatty acid concentration and the fecal microbial structure of weaned piglets. Our study laid a good foundation for the application of the novel coated nano zinc oxide in animals in the future. High dose of zinc oxide (ZnO) could improve growth performance and alleviate disease status, whereas it caused serious environmental pollution and bacterial resistance. This study was to investigate whether low doses of sodium alginate-coated nano zinc oxide (saZnO), a new type of zinc resource, could serve as a potential alternative to pharmacological doses of traditional ZnO in weaned piglets. A total of 144 crossbred piglets were randomly allocated into three groups, including a basal diet without the addition of Zn (CON), a basal diet with 1600 mg Zn/kg from traditional ZnO (ZnO), and a basal diet with 500 mg Zn/kg from saZnO (saZnO). The experiment lasted for 28 days. The results showed that supplementing with ZnO and saZnO for 14 and 28 days significantly improved body weight (BW) and average daily gain (ADG) (p < 0.01) and markedly reduced the feed intake-to-gain ratio (F/G) (p < 0.05) and diarrhea rate. In addition, dietary ZnO and saZnO significantly increased the activities of the total antioxidant capacity (T-AOC) and alkaline phosphatase (ALP) (p < 0.01). Supplementing with saZnO also promoted the levels of superoxide dismutase (SOD), IgM and copper- and zinc-containing superoxide dismutase (Cu/Zn-SOD) in serum (p < 0.05), whereas a ZnO addition decreased the concentration of malondialdehyde (MDA) (p < 0.05), indicating the beneficial effect of Zn on antioxidant and immune functions. Piglets fed the ZnO diet showed higher serum Zn accumulations than those fed the CON and saZnO diets at d 28 (p < 0.01), and supplementing with ZnO and saZnO markedly contributed to Zn excretion in feces, especially in the ZnO diet (p < 0.01). Additionally, piglets fed the saZnO diet had greater valeric acid concentrations (p < 0.05) in their feces, while other short chain fatty acids (SCFAs) were not affected by different treatments (p > 0.05). Microbial alpha diversity was reduced in the saZnO group compared with the CON group (p < 0.05), while an obvious separation of microbial composition, the marker of beta diversity, was shown among the three groups (p < 0.05). At the genus level, six genera, including Clostridium_sensu_stricto_1, Terrisporobacter, f_Muribaculaceae, Subdoligranulum and Intestinibacter, were pronouncedly increased in the ZnO and saZnO groups (p < 0.05); another nine species were dramatically downregulated, such as f_Lachnospiraceae, f_Prevotellaceae, f_Butyricicoccaceae and f_Ruminococcaceae (p < 0.05). Finally, a functional analysis indicated that altered microbes significantly changed the "Metabolism" pathway (p < 0.05). These findings suggested that saZnO could act as a feasible substitute for ZnO to reduce Zn emission and enhance growth performance, antioxidant and immune functions, and to adjust the structure of gut microbiota in piglets. [ABSTRACT FROM AUTHOR]

We previously found that Lactobacillus plantarum (LP)‐derived postbiotics protected animals against Salmonella infection, but the molecular mechanism remains obscure. This study clarified the mechanisms from the perspective of autophagy. Intestinal porcine epithelial cells (IPEC‐J2) were pretreated with LP‐derived postbiotics (the culture supernatant, LPC; or heat‐killed bacteria, LPB), and then challenged with Salmonella enterica Typhimurium (ST). Results showed that LP postbiotics markedly triggered autophagy under ST infection, as indicated by the increased LC3 and Beclin1 and the decreased p62 levels. Meanwhile, LP postbiotics (particularly LPC) exhibited a strong capacity of inhibiting ST adhesion, invasion and replication. Pretreatment with the autophagy inhibitor 3‐methyladenine (3‐MA) led to a significant decrease of autophagy and the aggravated infection, indicating the importance of autophagy in LP postbiotics‐mediated Salmonella elimination. LP postbiotics (especially LPB) significantly suppressed ST‐induced inflammation by modulating inflammatory cytokines (the increased interleukin (IL)‐4 and IL‐10, and decreased tumor necrosis factor‐α (TNF), IL‐1β, IL‐6 and IL‐18). Furthermore, LP postbiotics inhibited NOD‐like receptor protein 3 (NLRP3) inflammasome activation, as evidenced by the decreased levels of NLRP3, Caspase‐1 and apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC). Deficits in autophagy resulted in an increase of inflammatory response and inflammasome activation. Finally, we found that both LPC and LPB triggered AMP‐activated protein kinase (AMPK) signaling pathway to induce autophagy, and this was further confirmed by AMPK RNA interference. The intracellular infection and NLRP3 inflammasome were aggravated after AMPK knockdown. In summary, LP postbiotics trigger AMPK‐mediated autophagy to suppress Salmonella intracellular infection and NLRP3 inflammasome in IPEC‐J2 cells. Our findings highlight the effectiveness of postbiotics, and provide a new strategy for preventing Salmonella infection. [ABSTRACT FROM AUTHOR]

Chitosan nanoparticles (CNP), widely applied as oral drug/gene/vaccine carrier, were found to have anti‐inflammatory properties. In this study, the effects of CNP on lipopolysaccharide (LPS)‐induced intestinal damage in weaned piglets and the related mechanisms were investigated. Twenty‐four weaned piglets (Duroc × Landrace × Yorkshire, 21 ± 2 day of age, initial mass: 8.58 ± 0.59 kg) were randomly assigned into four groups: control, LPS, CNP and CNP + LPS. The control and LPS groups were fed a corn–soybean meal‐based control diet, whereas the CNP and CNP + LPS groups were fed a control diet supplemented with 400 mg/kg CNP. After 28 days of feeding, piglets in LPS and CNP + LPS groups were injected with LPS (100 μg/kg); meanwhile, the piglets in control and CNP groups were injected with sterile saline. After 4 h from the LPS challenge, pigs were sacrificed to collect the intestinal samples for analysis. The results showed that CNP could attenuate the intestinal damages and inflammatory response stimulated by LPS treatment. LPS induced dramatically higher levels of CD177+ neutrophils invasion in jejunum mucosa (p < 0.01), which accompanied by increased secretion of marks of inflammation (p < 0.01) compared with the control, whereas CNP administration obviously inhibited LPS‐induced CD177+ neutrophils invasion (p < 0.01) and secretion of marks of inflammation, such as interleukin‐8 (p < 0.05), intercellular adhesion molecule‐1 (p < 0.05) secretion in jejunum mucosa compared with LPS group. Moreover, CNP was shown to inhibit IκB‐α degradation in cytoplasm, which resulted in reduced nuclear translocation of NF‐κB p65 in LPS‐challenged piglets. These findings suggest that CNP attenuates intestinal damage and inflammatory responses in LPS‐challenged weaned piglets by impairing the NF‐κB signalling pathway. [ABSTRACT FROM AUTHOR]

Although a number of theories have been suggested, including roles for oxidative stress, an abnormal maternal‐fetal interface, and genetic and environmental factors, the etiopathology of pre‐eclampsia (PE) remains unclear. Maternal immune tolerance is important for maintaining pregnancy, and researchers have increasingly focused on the critical roles of cytokines in the pathogenesis of PE in recent years. The assessment of candidate genetic polymorphisms in PE could partially elucidate the mechanisms of susceptibility to disease, and contribute to seeking for new diagnosis and treatment methods of PE. PE can lead to severe complications, and even the death of both mother and fetus. Although the complex pathology is not yet clear, some evidence suggested that the occurrence of PE is related to inflammatory factors. We reviewed the current understandings of roles of cytokines in PE, and provided an extensive overview of the role of single nucleotide chain polymorphisms (SNPs) in the genes potentially underlying the pathophysiology of PE. [ABSTRACT FROM AUTHOR]