BackgroundFluoride which is widespread in our environment and food due to geological origin and industrial pollution has been identified as developmental neurotoxicants. Gut-brain axis provide new sight to the brain-derived injury. We hypothesized that fluoride-induced memory impairment was associated with gut dysbiosis, which could be prevented by improving the gut microbiota. MethodsMice were given fluoridated drinking water (sodium fluoride, 100 mg/L) for 70 days and administered with PBS or a probiotic strain, Lactobacillus johnsonii BS15 for 28 days prior to and throughout a 70 day exposure to sodium fluoride. ResultsResults showed that fluoride reduces the exploration ratio in Novel object recognition (NOR) test and the spontaneous exploration during the T-maze test in mice following an hour water avoidance stress (WAS), which were significantly improved by the probiotic. 16S rRNA sequencing showed a significant seperation in ileal microbiota between the fluoride-treated mice and control mice. Lactobacillus was the mainly targeting bacteria and significantly reduced in fluoride-treated mice. BS15 reconstructed the fluoride-post microbiota and increased the relative abundance of Lactobacillus. D-lactate contant and diamine oxidase (DAO) activity, two biomarkers of the gut permeability were reduced in the serum of probiotic-inocluated mice. ZO-1, an intestinal tight junction protein, which was reduced by fluoride in mRNA and protein levels were increased by the probiotic treatment. Moreover, in the hippocampus which is essential to learning and memory, the probiotic increased the down-regulated mRNA levels of myelinassociated glycoprotein (MAG) level, Bcl-xl and decreaed up-regulated mRNA levels of Bad in fluoride-treated mice. The probiotic applied in this study also increased down-regulated mRNA and protein levels of brain-derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB), and balanced the inflammatory cytokines in mRNA and protein levels in hippocampus of fluoride-treated mice. ConclusionsThese results suggested that there may be some correlations between the fluoride-induced memory dysfunction and alteration of gut microbiota, and reconstruction of gut microbiota is a potential method to prevent the memory dysfunction.
Cadmium (Cd) is known as a highly toxic heavy metal and has been reported to induce hepatotoxicity in animals. Nano-selenium (NSe) is an antioxidant that plays many biological roles such as oxidative stress alleviation. The purpose of this study is to explore the mechanism of action by which NSe inhibits Cd-induced hepatic toxicity and oxidative stress. Sixty eight-week-old male Kunming mice were randomly divided into four groups (15 mice per group). The control group and cadmium groups received distilled water, whereas the sodium-selenite group received 0.2 mg/kg SSe and the NSe group received 0.2 mg/kg NSe intragastrically for 2 weeks. On the last day, all the other groups were treated with Cd (126 mg/kg) except for the control group. The results obtained in this study showed that NSe alleviated Cd-induced hepatic pathological changes. Furthermore, NSe reduced the activities of ALT and AST as well as the content of MDA, while elevated the activities of T-AOC, T-SOD and GSH (P < 0.05). In addition, the NSe group significantly increased mRNA expressions of Nrf2 pathway related molecules (Nrf2, HO-1, NQO-1, GST, GSH-Px, CAT and SOD) compared to the Cd group (P < 0.05). In conclusion, NSe shows its potentiality to reduce Cd-induced liver injury by inhibiting oxidative stress and activating the Nrf2 pathway.
The continuous ovulation of laying hens during the peak period is likely to cause oxidative stress, resulting in a reduction in the laying cycle over time. The aim of this study was to evaluate the antioxidant effects of Aronia melanocarpa (AM) in the diet and its effect on the yolk precursor content caused by ovulation in laying hens during the peak period. A total of 300 25-week-old Roman brown laying hens were randomly divided into five groups with six replicates in each group, 10 in each replicate. The control group was fed a basal diet, the positive control group was fed a Vitamin C (VC) plus basal diet, and the experimental group was fed 1%, 4%, and 7% doses of AM plus diet according to the principle of energy and nitrogen requirements, which lasted eight weeks. At the end of the study, the egg quality, biochemical, and antioxidant markers, as well as mRNA and protein expressions, were evaluated to determine the potential signaling pathways involved. Results showed that the addition of AM to the feed increased the weight of laying hens at the peak of egg production and improved egg quality. The biochemical markers, as well as the antioxidant parameters in the serum, liver, and ovarian tissues, were ameliorated. The gene and protein expression of recombinant kelch-like ECH-associated protein 1 (Keap1) in the liver and ovarian tissues was decreased, while nuclear factor erythroid-2 related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression was increased. The feed supplemented with AM also increased the estrogen contents and lipid parameters, as well as the gene and protein expressions related to the yolk precursor. Feed supplemented with AM could improve the egg quality and the oxidative stress caused by the ovulation process of laying hens during the peak egg production period by activating the Keap1/Nrf2 signaling pathway. These results suggest that the feed supplemented with 1% AM and 4% AM can improve egg production in peak laying hens.
Background Tembusu virus (TMUV), a newly emerging pathogenic flavivirus, is acute and spreads rapidly which causes massive economic losses in the Chinese duck industry. Vaccination is the most effective method to prevent TMUV. So, it’s urgent to look for an effective vaccine strategy against TMUV. Heterologous prime-boost regimen priming with DNA vaccine and boosting with recombinant adenovirus vaccine have been proven to be the successful strategy in protecting against virus in experimental animal models. Methods In this study, heterologous and homologous prime-boost strategies using DNA vaccine and recombinant adenovirus vaccine expressing prM-E or E protein of TMUV were evaluated to protect ducks against the infection of TMUV for the first time, including priming and boosting with DNA vaccine, priming and boosting with recombinant adenovirus vaccine, and priming with DNA vaccine and boosting with recombinant adenovirus vaccine. Humoral and cellular immune responses were detected and evaluated. We then challenged the ducks with TMUV at 12 days after boosting to assay for the clinical symptoms, mortality, viral loads and histopathological lesions of these different strategies. Results Comparing with homologous prime-boost strategies, higher levels of specific antibodies against E protein and the neutralizing antibodies against TMUV were detected in heterologous prime-boost regimen. And also, it could induce higher levels of IFN-γ than homologous prime-boost strategies in the later stage. Interestingly, heterologous prime-boost strategy induced higher level of IL-4 in the early stage, but gradually decreased and was even lower than homologous prime-boost strategy in the later stage. Moreover, the heterologous prime-boost strategy could efficiently protect ducks with low viral tiers, no clinical symptoms and histopathological lesions in this experiment after challenging with TMUV while slight clinical symptoms and histopathological lesions were observed in homologous prime-boost strategies. Conclusions Our results indicated that the heterologous prime-boost strategy induced higher levels of humoral and cellular immune responses and better protection against the TMUV infection in ducks than the homologous prime-boost strategies, suggesting that heterologous prime-boost strategy is an important candidate for the design of a novel vaccine strategy against TMUV.
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