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Nickel and chromium are both common heavy metals that pose serious environmental and health hazards. However, the exact mechanism by which nickel and/or chromium cause renal injury is unclear. Therefore, we explored the molecular mechanisms of renal injury caused by nickel and/or chromium poisoning from the perspective of mitochondrial dynamics and the Nrf2 antioxidant pathway. In this study, eighty 6-week-old C57BL/6J mice were randomly divided into four groups: control (Con, untreated), nickel (Ni, 110 mg/L Ni2+), chromium (Cr, 50 mg/L Cr6+), and combined nickel–chromium (Ni + Cr, 110 mg/L Ni2+, 50 mg/L Cr6+). The results showed that chronic nickel and/or chromium exposure inhibited body weight gain and impaired kidney function and structure in mice. Chronic nickel and/or chromium exposure led to the disruption of mitochondrial dynamics and thus induced oxidative stress. On the other hand, the Nrf2 antioxidant pathway may play an important regulatory role in mitigating oxidative stress-induced oxidative damage in kidney. The present study partially elucidated the molecular mechanism of renal injury induced by nickel and/or chromium exposure in mice and the regulatory role of the Nrf2 pathway in inducing oxidative injury from the perspective of mitochondrial dynamics. This provides a theoretical basis for the development of prevention and control strategies, and environmental protection measures. [ABSTRACT FROM AUTHOR]

NIBV is an acute and highly contagious virus that has a major impact on the poultry industry. Wogonin, as a flavonoid drug, has antiviral effects, but there have been no reports indicating its role in renal injury caused by NIBV infection. The aim of this study is to investigate the antiviral effect of wogonin against NIBV. Renal tubular epithelial cells were isolated and cultured, and divided into four groups: Con, Con+Wog, NIBV and NIBV+Wog. We found that wogonin significantly inhibited the copy number of NIBV and significantly alleviated NIBV-induced cell apoptosis and necrosis. Moreover, wogonin inhibited the reduction in mitochondrial membrane potential and the aberrant opening of mPTP caused by NIBV. In conclusion, wogonin can protect renal tubular epithelial cells from damage by inhibiting the replication of NIBV and preventing mitochondrial apoptosis and necroptosis induced by NIBV. [ABSTRACT FROM AUTHOR]

Fatty liver hemorrhagic syndrome (FLHS) in laying hens is a nutritional metabolic disease commonly observed in high-yielding laying hens. Sodium butyrate (NaB) and ferroptosis were reported to contribute to the pathogenesis of fatty liver-related diseases. However, the underlying mechanism of NaB in FLHS and whether it mediates ferroptosis remains unclear. A chicken primary hepatocyte induced by free fatty acids (FFAs, keeping the ratio of sodium oleate and sodium palmitate concentrations at 2:1) was established, which received treatments with NaB, the ferroptosis inducer RAS-selective lethal 3 (RSL3), and the inhibitor ferrostatin-1 (Fer-1). As a result, NaB increased biochemical and lipid metabolism indices, and the antioxidant level, while inhibiting intracellular ROS accumulation and the activation of the ferroptosis signaling pathway, as evidenced by a reduction in intracellular iron concentration, upregulated GPX4 and xCT expression, and inhibited NCOA4 and ACSL4 expression. Furthermore, treatment with Fer-1 reinforced the protective effects of NaB, while RSL3 reversed it by blocking the ROS/GPX4/ferroptosis pathway, leading to the accumulation of lipid droplets and oxidative stress. Collectively, our findings demonstrated that NaB protects hepatocytes by regulating the ROS/GPX4-mediated ferroptosis pathway, providing a new strategy and target for the treatment of FLHS. [ABSTRACT FROM AUTHOR]

Berberine (BBR) is a natural alkaloid with multiple biotical effects that has potential as a treatment for fatty liver hemorrhagic syndrome (FLHS). However, the mechanism underlying the protective effect of BBR against FLHS remains unclear. The present study aimed to investigate the effect of BBR on FLHS induced by a high-energy, low-protein (HELP) diet and explore the involvement of the gut microbiota and bile acid metabolism in the protective effects. A total of 90 healthy 140-day-old Hy-line laying hens were randomly divided into three groups, including a control group (fed a basic diet), a HELP group (fed a HELP diet), and a HELP+BBR group (high-energy, high-protein diet supplemented with BBR instead of maize). Our results show that BBR supplementation alleviated liver injury and hepatic steatosis in laying hens. Moreover, BBR supplementation could significantly regulate the gut's microbial composition, increasing the abundance of Actinobacteria and Romboutsia. In addition, the BBR supplement altered the profile of bile acid. Furthermore, the gut microbiota participates in bile acid metabolism, especially taurochenodeoxycholic acid and α-muricholic acid. BBR supplementation could regulate the expression of genes and proteins related to glucose metabolism, lipid synthesis (FAS, SREBP-1c), and bile acid synthesis (FXR, CYP27a1). Collectively, our findings demonstrate that BBR might be a potential feed additive for preventing FLHS by regulating the gut microbiota and bile acid metabolism. [ABSTRACT FROM AUTHOR]

Hexavalent chromium (Cr(VI)) is a hazardous substance that poses significant risks to environmental ecosystems and animal organisms. However, the specific consequences of Cr(VI) exposure in terms of liver damage remain incompletely understood. This study aims to elucidate the mechanism by which Cr(VI) disrupts mitochondrial dynamics, leading to hepatic injury in ducks. Forty-eight healthy 8-day-old ducks were divided into four groups and subjected to diets containing varying doses of Cr(VI) (0, 9.28, 46.4, and 232 mg/kg) for 49 days. Our results demonstrated that Cr(VI) exposure resulted in disarranged liver lobular vacuolation, along with increasing the serum levels of ALT, AST, and AKP in a dose-dependent manner, which indicated liver damage. Furthermore, Cr(VI) exposure induced oxidative stress by reducing the activities of T-SOD, SOD, GSH-Px, GSH, and CAT, while increasing the contents of MDA and H2O2. Moreover, Cr(VI) exposure downregulated the activities of CS and MDH, resulting in energy disturbance, as evidenced by the reduced AMPK/p-AMPK ratio and PGC-1α protein expression. Additionally, Cr(VI) exposure disrupted mitochondrial dynamics through decreased expression of OPA1, Mfn1, and Mfn2 and increased expression of Drp-1, Fis1, and MFF proteins. This disruption ultimately triggered mitochondria-mediated apoptosis, as evidenced by elevated levels of caspase-3, Cyt C, and Bax, along with decreased expression of Bcl-2 and the Bcl-2/Bax ratio, at both the protein and mRNA levels. In summary, this study highlights that Cr(VI) exposure induces oxidative stress, inhibits the AMPK-PGC-1α pathway, disrupts mitochondrial dynamics, and triggers liver cell apoptosis in ducks. [ABSTRACT FROM AUTHOR]

This study aimed to understand the changes in the milk and gut microbiota of dairy cows with mastitis, and to further explore the relationship between mastitis and the microbiota. In this study, we extracted microbial DNA from healthy and mastitis cows and performed high-throughput sequencing using the Illumina NovaSeq sequencing platform. OTU clustering was performed to analyze complexity, multi-sample comparisons, differences in community structure between groups, and differential analysis of species composition and abundance. The results showed that there were differences in microbial diversity and community composition in the milk and feces of normal and mastitis cows, where the diversity of microbiota decreased and species abundance increased in the mastitis group. There was a significant difference in the flora composition of the two groups of samples (P < 0.05), especially at the genus level, the difference in the milk samples was Sphingomonas (P < 0.05) and Stenotrophomonas (P < 0.05), the differences in stool samples were Alistipes (P < 0.05), Flavonifractor (P < 0.05), Agathobacter (P < 0.05) and Pygmaiobacter (P < 0.05). In conclusion, the microbiota of the udder and intestinal tissues of dairy cows suffering from mastitis will change significantly. This suggests that the development of mastitis is related to the endogenous pathway of microbial intestinal mammary glands, but the mechanisms involved need further study. [ABSTRACT FROM AUTHOR]

Simple Summary: Energy deficiency causes multiple organ dysfunctions in the lipopolysaccharide (LPS)-induced model. Quercetin is a flavonoid found in many plants including herbal medicines; nevertheless, the protective effects of quercetin in alleviating LPS-induced energy deficiency remain unclear. In the present study, an in ovo LPS-induced inflammation model was established in chicken embryos. Quercetin attenuated the increase in glycogen and lipid contents in the liver after LPS stimulation when compared with the control group. Quercetin could downregulate the mRNA expressions of AMPKα1 and AMPKα2 in the duodena, ceca, and livers when compared with the LPS group; quercetin decreased the immunoreactivity to AMPKα2 in the duodena and livers. The LPS-induced high mRNA expressions of PPARα and SGLT1 were blocked by quercetin in the duodena, ceca, and livers. Quercetin improved the APOA4 decrease in the duodena, ceca, and livers after LPS induction. Quercetin could downregulate the mRNA expression of PEPT1 in the duodena and ceca increased after LPS challenge. These data demonstrate that quercetin improves the energy deficiency induced by LPS in chicken embryos. Energy deficiency causes multiple organ dysfunctions after LPS induction. Quercetin is a phenolic compound found in herbal medicines. However, the effects of quercetin in alleviating LPS-induced energy deficiency remain unclear. In the present study, an in vivo LPS-induced inflammation model was established in chicken embryos. Specific pathogen-free chicken embryos (n = 120) were allocated to control, PBS with or without ethanol, quercetin (10, 20, or 40 nmol, respectively), and LPS (125 ng/egg) with or without quercetin groups. Fifteen day old embryonated eggs were injected with the abovementioned solutions via the allantoic cavity. On embryonic day 19, the tissues of the embryos were collected for histopathological examination using frozen oil red O staining, RNA extraction, real-time quantitative polymerase chain reaction, and immunohistochemical investigations. The glycogen and lipid contents in the liver increased after LPS stimulation as compared with the PBS group, whereas quercetin decreased the accumulation as compared with the LPS group. The mRNA expressions of AMPKα1 and AMPKα2 in the duodena, ceca, and livers were upregulated after LPS induction as compared with the PBS group, while quercetin could downregulate these expressions as compared with the LPS group. The immunopositivity of AMPKα2 in the villus, crypt, lamina propria, tunica muscularis, and myenteric plexus in the duodena and in the cytoplasms of hepatocytes significantly increased after LPS induction when compared with the PBS group (p < 0.01), whereas the immunopositivity to AMPKα2 in the quercetin treatment group significantly decreased when compared with the LPS group (p < 0.01 or p < 0.05). The LPS-induced high expressions of transcription factor PPARα and glucose transporter (SGLT1) were blocked by quercetin in the duodena, ceca, and livers. Quercetin treatment improved the LPS-induced decrease in APOA4 in the duodena, ceca, and livers. The mRNA expression of PEPT1 in the duodena and ceca increased after LPS challenge, whereas quercetin could downregulate PEPT1 gene expression. These data demonstrate that quercetin improved the energy deficiency induced by LPS in chicken embryos. The LPS-induced inflammation model was established to avoid the effect of LPS exposure from the environment and intestinal flora. The results form the basis the administration of quercetin pretreatment (in ovo infection) to improve the energy state of chicken embryos and improve the inflammation response. [ABSTRACT FROM AUTHOR]

Oxidative stress can adversely affect the health status of the body, more specifically by causing intestinal damage by disrupting the permeability of the intestinal barrier. This is closely related to intestinal epithelial cell apoptosis caused by the mass production of reactive oxygen species (ROS). Baicalin (Bai) is a major active ingredient in Chinese traditional herbal medicine that has antioxidant, anti-inflammatory, and anti-cancer properties. The purpose of this study was to explore the underlying mechanisms by which Bai protects against hydrogen peroxide (H2O2)-induced intestinal injury in vitro. Our results indicated that H2O2 treatment caused injury to IPEC-J2 cells, resulting in their apoptosis. However, Bai treatment attenuated H2O2-induced IPEC-J2 cell damage by up-regulating the mRNA and protein expression of ZO-1, Occludin, and Claudin1. Besides, Bai treatment prevented H2O2-induced ROS and MDA production and increased the activities of antioxidant enzymes (SOD, CAT, and GSH-PX). Moreover, Bai treatment also attenuated H2O2-induced apoptosis in IPEC-J2 cells by down-regulating the mRNA expression of Caspase-3 and Caspase-9 and up-regulating the mRNA expression of FAS and Bax, which are involved in the inhibition of mitochondrial pathways. The expression of Nrf2 increased after treatment with H2O2, and Bai can alleviate this phenomenon. Meanwhile, Bai down-regulated the ratio of phosphorylated AMPK to unphosphorylated AMPK, which is indicative of the mRNA abundance of antioxidant-related genes. In addition, knockdown of AMPK by short-hairpin RNA (shRNA) significantly reduced the protein levels of AMPK and Nrf2, increased the percentage of apoptotic cells, and abrogated Bai-mediated protection against oxidative stress. Collectively, our results indicated that Bai attenuated H2O2-induced cell injury and apoptosis in IPEC-J2 cells through improving the antioxidant capacity through the inhibition of the oxidative stress-mediated AMPK/Nrf2 signaling pathway. [ABSTRACT FROM AUTHOR]

It is well established that PRRSV elimination is an effective strategy for PRRS control, but published reports concerning successful PRRSV elimination cases in farrow-to-finishing herds are rare. Here, we have reported a successful PRRSV elimination case in a farrow-to-finish herd by employing a "herd closure and rollover" approach with some modifications. Briefly, the introduction of pigs to the herd was stopped and normal production processes were maintained until the herd reached a PRRSV provisional negative status. During the herd closure, strict biosecurity protocols were implemented to prevent transmission between nursery pigs and sows. In the current case, introducing gilts before herd closure and live PRRSV exposure were skipped. In the 23rd week post-outbreak, the pre-weaning piglets started to show 100% PRRSV negativity in qPCR tests. In the 27th week, nursery and fattening barns fully launched depopulation. In the 28th week, nursery and fattening houses reopened and sentinel gilts were introduced into gestation barns. Sixty days post-sentinel gilt introduction, the sentinel pigs maintained being PRRSV antibody negative, manifesting that the herd matched the standard of the provisional negative status. The production performance of the herd took 5 months to bounce back to normal. Overall, the current study provided additional information for PRRSV elimination in farrow-to-finish pig herds. [ABSTRACT FROM AUTHOR]

The accumulation of copper (Cu) in the organisms could lead to kidney damage by causing mitochondrial dysfunction. Given that mitochondria are one of the targets of Cu poisoning, this study aimed to investigate the role of mitophagy in Cu‐induced mitochondrial dysfunction in renal tubular epithelial cells to understand the mechanism of Cu nephrotoxicity. Hence, the cells were treated with different concentrations of Cu sulfate (CuSO4) (0, 100, and 200 μM), and mitophagy inhibitor (Cyclosporine A, 0.5 μM) and/or 200 μM CuSO4 in the combination for 12 h. Results showed that Cu caused mitochondrial swelling, vacuoles, and cristae fracture; increased the number of mitochondrial and lysosome fluorescent aggregation points; upregulated the mRNA levels of mitophagy‐associated genes (LC3A, LC3B, P62, BNIP3, NIX, OPTN, NDP52, Cyp D LAMP1, and LAMP2) and protein levels of LC3II/LC3I, BNIP3, and NIX, downregulated the mRNA and protein levels of P62; reduced the mitochondrial membrane potential (MMP), ATP content, mitochondrial respiratory control rate (RCR), mitochondrial respiratory control rate (OPR), and the mRNA and protein levels of PGC‐1α, TOMM20, and Mfn2, but increased the mRNA and protein levels of Drp1. Besides, cotreatment with Cu and CsA dramatically decreased the level of mitophagy, but increased mitochondrial division, further reduced MMP, ATP content, RCR, and OPR, mitochondrial fusion and thereby reduced mitochondrial biogenesis. Taken together, these data indicated that Cu exposure induced BNIP3/NIX‐dependent mitophagy in duck renal tubular epithelial cells, and inhibition of mitophagy aggravated Cu‐induced mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

Simple Summary: Avian colibacillosis is one of the major causes of animal death and egg-production decline, which has caused economic losses to the poultry industry. When encountering avian colibacillosis, many poultry farms tend to use antibiotics to reduce losses. Additionally, the utilization of antimicrobials is also disputable. Our study shows that luteolin can alleviate the inflammation and oxidative stress caused by Escherichia coli in the ilea of chicks and may be used as a substitute for antibiotics to control avian colibacillosis. Avian pathogenic E. coli (APEC) is typically the cause of avian colibacillosis, which can result in oxidative stress, inflammation, and intestinal damage (APEC). Luteolin, in the form of glycosylation flavone, has potent anti-inflammatory and anti-oxidative properties. However, its effects on APEC-induced intestinal oxidative stress and NF-κB-mediated inflammation in chicks remains poorly understood. After hatching, one-day-old chicks were stochastically assigned to four groups: a control group (basic diet), an E. coli group (basic diet) and L10 and L20 groups (with a dry matter of luteolin diet 10 mg/kg and 20 mg/kg, respectively), with fifteen chicks in each group and one repeat per group. They were pretreated for thirteen days. The body weight, mortality, histopathological changes in the ileum, antioxidant status, and the mRNA and protein-expression levels of factors associated with the HMGB1/TLR4/NF-κB signal axis of the chicks were measured. The results showed that luteolin treatment decreased the mRNA and protein-expression level of the related factors of HMGB1/TLR4/NF-κB signal axis in the ileum, reduced inflammation, increased antioxidant enzyme activity, and reduced intestinal injury. Collectively, luteolin alleviated APEC-induced intestinal damage by means of hindering the HMGB1/TLR4/NF-κB signal axis, which suggests that luteolin could be a good method for the prevention and treatment of avian colibacillosis. [ABSTRACT FROM AUTHOR]

Simple Summary: Diarrhea has been a global health problem for centuries, and its treatment has become increasingly difficult due to the antibiotics overuse and resistance. Quercetin is a common flavonoid of extracts of vegetables, fruits, and traditional Chinese herbs, however, the mechanism of quercetin alleviating LPS-induced duodenal inflammation remains elusive. The results demonstrated quercetin enhanced the inflammatory cell infiltration in the Peyer's patch of the intestinal mucosa after LPS induction. The LPS-induced expressions of these inflammation-related factors were completely blocked by quercetin. Quercetin also decreased the protein expression of inflammatory factors after LPS induction. Quercetin could down-regulate autophagy gene expression, and decreased the protein expression after LPS induction. Quercetin treatment prevented LPS-induced increases in the gene expressions of programmed cell death factors; meanwhile, quercetin decreased the protein expression of caspase 1 and caspase 3 after LPS challenge. LPS reduced the gene expression of mucin 2, but upregulated the mRNA and protein expression of claudin 1, occludin, and ZO-1, which was balanced by quercetin. These evidences suggest quercetin can alleviate duodenal inflammation induced by LPS through modulating autophagy, programmed cell death, and intestinal barrier function. Diarrhea has been a global health problem for centuries, and the treatment has become increasingly difficult duo to the antibiotics overuse and resistance. Quercetin is a common flavonoid of extracts of vegetables, fruits, and traditional Chinese herbs, however, the mechanism of quercetin alleviating LPS-induced duodenal inflammation remains elusive. Specific pathogen-free chicken embryos (n = 120) were allocated to groups including control, PBS with or without alcohol, LPS (125 ng/egg) with or without quercetin (10, 20, or 40 nmol/egg, respectively), and quercetin groups (10, 20, or 40 nmol/egg). Fifteen day-old embryonated eggs were inoculated with abovementioned solutions via the allantoic cavity. At embryonic day 19, the duodena of the embryos were collected for histopathological examination, RNA extraction and real-time polymerase chain reaction, immunohistochemical investigations, and Western blotting. The results demonstrated quercetin enhanced the inflammatory cell infiltration in the Peyer's patch of the intestinal mucosa after LPS induction. The LPS-induced expressions of these inflammation-related factors (TLR4, IL-1β, MMP3, MMP9, NFKB1, IFNγ, IL-8, IL-6) were completely blocked by quercetin. Quercetin also decreased the protein expression of TLR4, IL-1β, MMP3, and MMP9 after LPS induction. Quercetin could down-regulate autophagy gene expression (ATG5, LC3-1, LC3-2, and LKB1), and decreased the protein expression of ATG5, and LC3-1/LC3-2 after LPS induction. Quercetin treatment prevented LPS-induced increases of the gene expressions of programmed cell death factors (TNFα, Fas, CASP1, CASP3, CASP12, Drp1, and RIPK1); meanwhile, quercetin decreased the protein expression of CASP1 and CASP3 after LPS challenge. LPS reduced the gene expression of mucin 2, but upregulated the mRNA and protein expression of claudin 1, occludin, and ZO-1, and this was balanced by quercetin. This evidence suggests that quercetin can alleviate duodenal inflammation induced by LPS through modulating autophagy, programmed cell death, intestinal barrier function. [ABSTRACT FROM AUTHOR]

The present study evaluated the nutritional values and in vitro fermentation characteristics of 29 different Chinese herbs in order to develop effective feed additives for livestock nutrition. The Chinese herbs were analyzed for their chemical composition. The in vitro fermentation characteristics were evaluated using the gas production technique with swine cecal chyme inoculum. The results showed that the Allium tuberosum Rottl (Semen allii tuberosi, SAT) had the highest gross energy (GE), crude protein (CP), ether extract (EE), and total amino acid (TAA) contents, whereas Anemones raddeanae Rhizoma (Agstache rugosus, AR) had the highest crude fiber, neutral detergent fiber, and acid detergent fiber contents compared with the other Chinese herbs. The Rhus chinensis Mill (Chinese gall, CG), Scrophularia ningpoensis Hemsl (Radix scrophulariae, RS), Punica granatum L (Punica granatum L, PGL), Atractylodes macrocephala Koidz (White atractylodes rhizome, WAR), Sanguisorbae radix (Garden burnet, GB), Anemarrhena asphodeloides Bunge (Rhizoma anemarrhenaw, RA), and Rhei radix Et Rhizoma (Rheum officinale, RO) had a higher non-fiber carbohydrate content than the other Chinese herbs. The in vitro fermentation kinetic analysis showed that the RS, WAR, and RA had a higher gas production, a theoretical gas production, and a fractional rate of gas production than the other groups. Furthermore, the RA, WAR, RS, and Crataegi fructus (Crataegus pinnatifida Bun, CPB) had a higher total short-chain fatty acids (SCFAs) concentration, and CPB had the highest acetate concentration, whereas the WAR and RS had higher propionate and butyrate concentrations than the other groups. Moreover, the Isatis indigotica Fort (Folium isatidis, FI) and SAT had higher ammonia-N concentration than the other groups. In summary, among the 29 different Chinese herbs, the SAT had the highest nutritional value, which is reflected in the highest contents of GE, CP, EE, and TAA, whereas the RA, WAR, and RS showed better intestinal fermentation profiles, which is reflected in the higher fermentation degree and suitable SCFAs fermentation pattern. These findings provide a theoretical basis for using Chinese herbs as feed additives or microbial carbon sources in the intestines of animals. [ABSTRACT FROM AUTHOR]

Metabolism-associated fatty liver disease (MAFLD) is one of the most common causes of liver disease; however, the underlying processes remain unknown. This study aimed to investigate the changes of free fatty acids (FFA) on the expression of genes related to the AMP-activated protein kinase (AMPK) signaling pathway in the primary hepatocytes of laying hens. The primary hepatocytes of laying hens were treated with FFA (containing a 2:1 ratio of oleic and palmitic acids) for 24 h. FFA significantly increased lipid droplet accumulation, decreased glycogen synthesis, increased the levels of triglycerides (TG), total cholesterol (TC), reactive oxygen species (ROS), malondialdehyde (MDA), and glucose content in the supernatant (GLU) in the primary hepatocytes of laying hens, and decreased the levels of total antioxidant capacity (T-AOC) and superoxide dismutase (SOD), as well as mitochondrial membrane potential (MMP). The results of the PCR array combined with Western blotting experiments showed that the activity of AMPK was inhibited. Inhibition of AMPK signaling pathway decreases the expression of genes involved in fatty acid oxidation, increases the expression of genes involved in lipid synthesis, decreases the expression of genes involved in glycogen synthesis, increases the expression of genes involved in glycolysis, increases the expression of genes involved in oxidative stress, and increases the expression of genes involved in cell proliferation and apoptosis. Taken together, our results suggest that FFA can affect the homeostasis of the AMPK signaling pathway by altering energy metabolic homeostasis, inducing oxidative stress, and adjusting the onset of cell proliferation and apoptosis. [ABSTRACT FROM AUTHOR]