BACKGROUND:To recover endangered green peafowl (Pavo muticus) populations, China has implemented ex situ conservation programs centered on captive breeding. However, captive-bred individuals frequently suffer from skeletal deformities, creating a critical bottleneck that compromises future wild reintroductions. RESULTS:This study demonstrates that, although green peafowl possess species-specific genes (Igf2 and Ndufs2), they lack specialized allometric development of the cecum, suggesting that dietary disparities might play a more pivotal role in driving skeletal issues than innate intestinal anatomical factors. Specifically, wild peafowl naturally consume plants from the genus Pistacia, whereas captive birds receive a standardized diet dominated by Glycine. Reflecting these dietary disparities, captive-bred individuals exhibit significantly reduced gut levels of metabolites that regulate osteoclast activity, namely quercetin, taurine, urolithin A, and luteolin. Extensive evidence indicates that these specific metabolites directly modulate bone homeostasis during growth, meaning their reduction poses severe physiological risks. Furthermore, the abundance of these specific metabolites is directly modulated by gut bacterial communities, notably the genera Escherichia and Staphylococcus. We also found that dietary composition serves as a robust cue shaping gut microbiome assembly, acting independently of developmental stages. CONCLUSIONS:This study suggests that targeted plant supplementation holds promise in restoring the gut ecosystem and mitigating skeletal deformities, highlighting how diet-driven microbiome stewardship could advance the conservation and reintroduction of endangered species like the green peafowl.

Background: The global dissemination of multidrug-resistant (MDR) Salmonella poses a persistent and serious threat to food safety systems. As a leading poultry-exporting country, Thailand requires a comprehensive understanding of how resistance plasmids spread among Salmonella populations within its chicken production chain. Methods: Between March 2023 and February 2024, 223 Salmonella isolates were collected from chicken slaughterhouses and markets in northeastern Thailand. From these, 19 representative MDR Salmonella enterica isolates, selected based on distinct spatiotemporal distributions, underwent whole-genome sequencing. Genomic analyses included sequence typing, core-genome phylogenetics, and screening for antimicrobial resistance genes. Plasmid replicons were identified, and functional annotation was performed using the COG database. Results: Phylogenetic analysis revealed 11 distinct sequence types within the population. Among these, ST1541 and ST50 showed clear evidence of clonal transmission across different production stages, with a notable clustering pattern observed during the winter season. All sequenced isolates exhibited an MDR phenotype. Plasmids were detected in 78.9% of isolates, with conjugative plasmids being the most frequent type (57.9%). The β-lactamase gene blaTEM-60 was the most prevalent (78.9%) and showed a strong correlation (r ≥ 0.7) with resistance to both ampicillin and cefotaxime. Functional annotation further revealed an abundance of genes involved in carbohydrate and amino acid metabolism across all isolates. Conclusions: These findings indicate that MDR Salmonella dissemination is driven by two synergistic mechanisms: the clonal expansion of fit lineages and the horizontal transfer of conjugative plasmids harboring β-lactamase genes. We identified IncI-gamma-K1 and Col-related plasmids as key vectors in this process. This study advocates for targeted interventions, guided by a One Health approach, that specifically aim to disrupt plasmid transmission at critical control points, such as slaughterhouses, to curb the spread of antimicrobial resistance.

Porcine pseudorabies virus (PRV) causes astrocyte injury through oxidative stress, inflammatory responses, and metabolic dysfunction. Rhynchophylline (RHY) possesses antioxidant and anti-inflammatory properties, but its protective effects against PRV infection remain unclear. Using PRV-infected C8-D1A cells, we evaluated the antiviral and cytoprotective effects of RHY. At a non-toxic concentration of 5 μM, RHY significantly inhibited PRV replication, reduced intracellular reactive oxygen species, and alleviated oxidative stress by decreasing xanthine oxidase (XOD), myeloperoxidase (MPO), malondialdehyde (MDA), and nitric oxide (NO) levels while restoring superoxide dismutase (SOD) activity. RHY also modulated PRV-induced inflammatory imbalance by suppressing interleukin (IL)-6 and IL-8 and enhancing IL-4 and IL-10 expression. Metabolomic profiling revealed that PRV infection disrupted cellular metabolism, particularly pathways related to unsaturated fatty acid biosynthesis and the tricarboxylic acid (TCA) cycle, which were largely restored by RHY treatment. These findings indicate that RHY exerts antiviral, anti-inflammatory, and antioxidant effects by correcting PRV-induced metabolic disturbances in vitro.

Pseudorabies virus (PRV) infection leads to viral encephalitis and neurological damage in mice, causing significant neurological symptoms and brain damage. This study aimed to investigate the cellular mechanisms of PRV-induced encephalopathy and the role of matrix metalloproteinase-9 (MMP-9) in blood–brain barrier (BBB) disruption. We found that PRV infection increased the number of astrocytes and induced a phenotypic shift from the A2 to the A1 subtype, which was associated with increased secretion of MMP-9. MMP-9 was identified as a critical mediator of PRV-induced BBB disruption, as it degrades collagen VI, leading to BBB damage. PRV was shown to penetrate the BBB via a paracellular pathway, and MMP-9 deletion reversed this damage, mitigating tight junction injury. Additionally, PRV infection caused an “inflammatory storm” in the central nervous system (CNS), with increased levels of the chemokines CCL-3, CCL-4, and CCL-5; the cytokines IL-6 and IL-18; and TNF-α. The expression of INF-γ was significantly decreased. In conclusion, PRV infection disrupts the BBB and induces an inflammatory response in the CNS, with MMP-9 playing a key role in mediating BBB damage. These findings provide insights into the pathogenesis of PRV-induced encephalopathy and potential therapeutic targets for viral encephalitis.

Pseudorabies virus (PRV) is known to induce severe reproductive disorders, yet the molecular mechanisms underlying testicular damage remain unclear. This research aims to explore the impact of PRV infection on porcine testicular (ST) cells and murine testicular tissue, with a focus on the involvement of the FOXO signaling pathway. This study also evaluated the antagonistic effect of compound RS on PRV infection through regulation of this pathway. Analyze differentially expressed genes and enriched pathways in ST cells infected with PRV through transcriptome sequencing. ST cells were infected with PRV and subsequently treated with either the FOXO pathway inhibitor AS1842856 or varying concentrations of RS (12.5, 25, and 50 μg/mL) to evaluate their effects on viral replication and FOXO gene expression. Cell viability was detected by CCK-8, viral load and mRNA expression of FOXO were detected by qPCR. Establish a PRV infected mouse model, observe pathological changes in testicular tissue through HE staining, detect testicular virus concentration, sperm count, and FOXO gene expression. PRV infection caused significant cytopathic effects in ST cells, with transcriptome sequencing identifying 1,650 significantly upregulated genes and 1,359 significantly downregulated genes (|log2FC| ≥ 1, P < 0.01). KEGG pathway analysis indicated significant enrichment of these genes in the FOXO signaling pathway, among others. Inhibition of the FOXO pathway markedly reduced viral replication in ST cells. PRV infection upregulated FOXO1 and FOXO4 mRNA expression, while downregulating FOXO3; these alterations were reversed upon RS treatment. In vivo experiments, RS treatment alleviated the pathological damage of mouse testicular tissue caused by PRV, reduced virus concentration in the testes, and partially restored sperm count. Compound RS effectively suppresses PRV replication both in vitro and in vivo by modulating the FOXO pathway and alleviates testicular injury caused by PRV. These findings provide a theoretical basis and identify a promising candidate for developing novel therapeutics targeting PRV-associated reproductive toxicity. Keywords: Rodgersia sambucifolia hemsl flavon; Scutellaria polysaccharide; Pseudorabies virus; FOXO signaling pathway

Erigeron breviscapus (Vant.) Hand-Mazz possesses anti-inflammatory and antioxidant properties, yet its therapeutic application is limited by the low yield of active components. Fermentation technology offers a promising strategy for enhancing the enrichment of these bioactive compounds. In this study, anaerobic self-induced fermentation was identified as the most effective approach among 12 evaluated fermentation strategies. Under optimized conditions, this method markedly increased the production of scutellarein—achieving a 20.35-fold enhancement—while reducing microbial α-diversity and inducing notable community restructuring, characterized by a shift from Proteobacteria to Firmicutes in bacteria and from Ascomycota to Basidiomycota in fungi. Metabolomic analysis revealed 223 differentially expressed metabolites, primarily enriched in flavonoid biosynthesis and phenylalanine metabolism pathways. Key bacterial genera, including Clostridium and Bacillus, showed strong correlations with increased flavonoid accumulation. Furthermore, the anaerobically self-fermented extract exhibited significantly enhanced antibacterial and antioxidant activities. These findings demonstrate that anaerobic self-induced fermentation represents an effective and targeted bioprocessing strategy for amplifying the bioactivity and therapeutic potential of E. breviscapus.

The development of field-deployable diagnostic tools for pseudorabies virus (PRV) surveillance remains challenging due to the technical limitations of conventional detection methods, particularly their reliance on sophisticated equipment and inadequate sensitivity for gE gene identification in resource-limited settings. To address these critical needs, we established a novel nucleic acid detection platform that synergistically integrates recombinase-aided amplification (RAA) with CRISPR-Cas12a technology. Through systematic optimization of four CRISPR RNAs (crRNAs) and corresponding primer sets targeting conserved regions of the PRV gE gene, validated by fluorescence quantification and electrophoretic analysis, we developed a rapid detection system capable of achieving 10 copies/μL sensitivity within 45 min under isothermal conditions (37 °C). Clinical validation demonstrated complete diagnostic concordance with standard PCR methods, successfully identifying all 11 positive specimens from 30 clinical samples. The platform’s technical innovation lies in its sequential reaction activation mechanism that enables single-tube operation, effectively eliminating aerosol contamination risks while maintaining reaction efficiency. Detection outcomes can be interpreted through dual modalities—real-time fluorescence monitoring for quantitative analysis and lateral flow strips for visual readouts significantly enhancing field applicability. Notably, this system exhibits a 1,000-fold sensitivity improvement compared to conventional PCR, establishing itself as a robust solution for point-of-care PRV monitoring with particular utility in veterinary settings lacking advanced laboratory infrastructure.

Background: Pseudorabies virus (PRV), a zoonotic swine alphaherpesvirus, poses a severe threat to global pig production and public health. Aim: This study aimed to investigate the regulatory role of the RASSF6 gene in PRV-infected porcine alveolar macrophages (3D4/21). Methods: We established stable cellular models of RASSF6 overexpression (verified by qRT-PCR and immunofluorescence using an empty vector control) and siRNA-mediated RASSF6 silencing (verified by qRT-PCR) to investigate the role of RASSF6. Using these models, we assessed viral replication (quantified by qRT-PCR/TCID50) and apoptosis (analyzed by flow cytometry with Annexin V/PI staining and ELISA). Results: RASSF6 expression was significantly upregulated after PRV infection. RASSF6 overexpression inhibited 3D4/21 cell proliferation and PRV replication and promoted apoptosis through Bax and Caspase-3/9 activation. RASSF6 silencing promoted cell proliferation and viral replication and inhibited apoptosis. Conclusion: RASSF6 is a critical host defense factor against PRV infection in porcine alveolar macrophages. RASSF6 upregulation restricts viral replication by inducing apoptosis via Bax/caspase-3/9 activation and simultaneously suppressing cell proliferation. Conversely, RASSF6 silencing creates a permissive environment for PRV propagation by inhibiting apoptosis and enhancing cell survival. These findings reveal RASSF6-mediated apoptosis as a novel antiviral mechanism and highlight its potential as a therapeutic target for controlling PRV pathogenesis.

Porcine epidemic diarrhea virus (PEDV) is a highly contagious pathogen responsible for devastating enteric disease and lethal watery diarrhea, leading to significant economic losses in the global swine industry. Understanding the epidemiology and genetic diversity of PEDV over the past decade is crucial for the effective prevention and treatment of porcine epidemic diarrhea. In this study, 1851 fecal samples were collected from pigs exhibiting diarrhea symptoms across 11 cities in Yunnan Province between 2013 and 2022. The prevalence of PEDV, along with other common swine diarrhea viruses, including porcine transmissible gastroenteritis virus (TGEV), porcine rotavirus (PoRV), porcine Sapporo virus (PoSaV), porcine stellate virus (PaStV), and porcine delta coronavirus (PDCoV) was assessed using a polymerase chain reaction (PCR) assay. The results revealed a total detection rate of 52.94% (980/1851) for the six viruses, with PEDV accounting for 25.93% (480/1851) of cases. Further analysis showed that weaned piglets were more susceptible to PEDV than fattening pigs, with the highest prevalence observed in spring (61.52%, 275/447) and the lowest in summer (12.68%, 97/765). Dual infections were also identified, with PEDV + PoSaV being the most common combination (2.81%, 52/1851), followed by PEDV + PoRV, with a detection rate of 1.67% (31/1851). Phylogenetic analysis of the PEDV S genes revealed that the 28 epidemic strains in Yunnan Province shared a nucleotide sequence homology from 91.4% to 98.4% and an amino acid sequence homology ranging from 85.6% to 99.3%. All strains were classified as GII variant strains. This study provides a comprehensive overview of the epidemiology of PEDV and its co-infection patterns with other common diarrhea-causing viruses in the swine herds of Yunnan Province over the past decade. These findings offer valuable insights for the development of effective prevention and control strategies to mitigate the impact of PEDV and other enteroviruses on the swine industry in Yunnan Province.

Aim of the studyThis study aimed to evaluate the protective effects of Glycyrrhiza polysaccharides (GPs) on Pseudorabies virus (PRV)-infected mice and elucidate their mechanisms of action, with a focus on intestinal immunity, oxidative stress, mucosal barrier function, and gut microbiota composition.Materials and methodsGPs were extracted via hot water extraction and ethanol precipitation. Seventy-two SPF-grade male mice were randomly divided into six groups and treated with different doses of GPs or Astragalus polysaccharides (APS), followed by PRV challenge. Clinical parameters, inflammatory cytokines (TNF-α, IL-6, IL-4, IL-10), oxidative stress markers (SOD, CAT, MDA), histopathology, tight junction protein expression (Occludin, ZO-1), sIgA levels, intestinal permeability, viral load, and gut microbiota profiles were assessed.ResultsGP administration significantly alleviated PRV-induced symptoms, reduced mortality and disease activity index, and improved food intake. Medium and high doses notably downregulated TNF-α and IL-6, while upregulating IL-4 and IL-10. Antioxidant activities (SOD, CAT) were enhanced, and MDA levels were decreased. Histological analyses showed recovery from villus atrophy and goblet cell loss. GPs improved tight junction integrity, elevated sIgA, reduced gut permeability and viral burden. Microbiota analysis revealed increased α-diversity, enrichment of Lactobacillus and Bacteroides, and suppression of potential pathogens. Functional predictions suggested GPs influenced immunity- and metabolism-related microbial pathways.ConclusionGPs exert protective effects against PRV-induced intestinal injury by modulating immune and oxidative responses, enhancing mucosal barrier integrity, and rebalancing gut microbiota. These findings support the potential of GPs as a therapeutic agent for viral enteric diseases. To our knowledge, this is the first study to demonstrate the protective role of GPs against PRV infection in vivo. These findings expand current understanding of the antiviral potential of plant-derived polysaccharides and highlight GPs as a promising candidate for the development of novel polysaccharide-based therapeutics for viral enteric diseases.

Scutellarin, the active component of Erigeron breviscapus(Vant.)Hand.-Mazz, has therapeutic potential for neurological diseases but is limited by poor solubility, low bioavailability, and inability to cross the blood-brain barrier (BBB). This study used mouse brain tissue-derived exosomes as a delivery system for scutellarin. Exosomes were isolated via ultracentrifugation and loaded with scutellarin using ultrasonication, achieving a drug loading capacity of 31.86 ng/μg and a particle size of 90-120 nm. In an in vitro BBB model, exosome-loaded scutellarin showed significantly higher penetration (41 %) than the free drug (13.5 %). Confocal microscopy confirmed efficient cellular uptake, particularly by microglia (98 % efficiency). In vivo, exosomes accumulated and persisted in brain tissue for over 24 h. In a PRV-infected microglia model, exosome-delivered scutellarin significantly inhibited viral replication and modulated microglial polarization by downregulating the pro-inflammatory marker CD86 and upregulating the anti-inflammatory marker CD206. These findings demonstrate that brain-derived exosomes enhance scutellarin delivery across the BBB and improve its anti-neuroinflammatory effects, supporting their use as drug carriers for treating neuroinflammatory diseases.

Background:Cyclophosphamide (CTX) is a widely used chemotherapeutic agent; however, its clinical application is often limited by significant reproductive toxicity, particularly testicular damage. Baicalin (BAI) has demonstrated broad pharmacological activities, including anti-inflammatory, antioxidant, and anti-apoptotic effects. Aim:To investigate the protective effect of BAI on testicular damage induced by CTX in rats. Methods:Network pharmacology was used to identify the core targets of BAI-testis damage. Animal experiments were conducted using 30 SPF-grade 7-week-old SD rats divided into a control group (Control), a CTX group, a low-dose BAI group (BAI-L), a medium-dose BAI group (BAI-M), and a high-dose BAI group (BAI-H), with six rats in each group. Molecular docking, quantitative polymerase chain reaction, and Western blot were used to validate the core targets of network pharmacology. H&E staining was performed to observe testicular tissue damage. The levels of interleukin-1β, interleukin-10, reactive oxygen species, and malondialdehyde in the testes and the levels of follicle-stimulating hormone, luteinizing hormone, and testosterone in the serum were measured. Immunofluorescence was used to detect germ, supporting, and interstitial cells in the testes. Results:Network pharmacology identified 127 common targets between BAI and testicular damage. BAI acts on Ptgs2, Gsk3b, and Pparg targets. Molecular docking and animal experiments indicated that BAI exhibits strong binding affinity with Ptgs2, Gsk3b, and Pparg. Animal experiments showed that BAI can improve CTX-induced pathological tissue damage, reduce inflammatory responses, and alleviate oxidative stress in rat testes. BAI can repair CTX-induced damage to germ cells, supporting cells, interstitial cells, and repaired reproductive hormones, with the extent of repair showing a dose-dependent relationship. Conclusion:This study demonstrates the beneficial effects of BAI in alleviating CTX-induced reproductive toxicity, and BAI can be used to reduce the side effects of CTX.

Erigeron breviscapus exhibits anti-inflammatory properties, protects neuronal cells and enhances immune function. Modern traditional Chinese medicine fermentation techniques can increase the bioactive compound content in Erigeron breviscapus. However, its potential therapeutic effects against the porcine pseudorabies virus (PRV) remain unclear. A PRV infection model was established in mouse trigeminal ganglion (TG) cells to determine the optimal antiviral mode of action of flavonoids from fermented Erigeron breviscapus (FEBF). Additionally, a PRV-infected rat model was developed to evaluate the in vivo antiviral efficacy of FEBF. FEBF demonstrated a higher protective rate and a lower viral copy number compared to unfermented E. breviscapus flavonoids (EBF). The protective effect was most pronounced under toxicological and inhibitory conditions, surpassing the blocking effect. PRV infection upregulated TLR4, MyD88, and NF-κB p65 protein expression during the pre-infection phase, followed by their downregulation after 12 h. FEBF regulated PRV-induced changes in protein expression, restoring them to near-normal levels by 36 h. In vivo assessments of pathological injury, PRV viral load, neuronal count, and neuronal apoptosis indicated that FEBF provided superior neuroprotection compared to both Minocycline (MINO), a broad-spectrum neuroprotective drug, and unfermented EBF. Mechanistic studies further revealed that FEBF modulated microglial polarization and regulated the inflammatory cytokines IL-6, TNF-α, IL-4, and IL-10. These findings demonstrate that FEBF exhibits significant antiviral effects against PRV in both in vitro and in vivo models. FEBF represents a promising candidate for the development of anti-PRV therapeutics.

Porcine pseudorabies has long existed in China and is a serious threat to the Chinese farming industry. To understand the prevalence and genetic variation of the porcine pseudorabies virus (PRV) and its pathogenicity in Yunnan Province, China, we collected 560 serum samples across seven Yunnan Province regions from 2020 to 2021 and detected anti-gE antibodies in these samples. Sixty-one clinical tissue samples were also collected from pigs with suspected PRV that were vaccinated with Bartha-K61. PRV-gE antibodies were found in 29.6% (166/560) of the serum samples. The PRV positivity rate in clinical tissue samples was 13.1% (8/61). Two isolates, PRV-KM and PRV-QJ, were obtained. The identity of the gB, gD, and gE genes between these isolates and the Chinese mutants exceeded 99.5%. These isolates and the classical Fa strain were used to infect 4-week-old rats intranasally to assess their pathogenicity. All infected rats showed the typical clinical and pathological features of PRV two days post-infection. The viral loads in the organs differed significantly among the infected groups. Viruses were detected in the saliva and feces at 12 h. Significant dynamic changes in total white blood cell counts (WBC), lymphocyte counts (Lym), and neutrophil counts (Gran) occurred in the blood of the infected groups at 24 and 48 h. These results show that mutant PRV strains are prevalent in Bartha-K61-vaccinated pigs in Yunnan Province, China. Moreover, rats shed PRV in their saliva and feces during early infection, indicating the need for rodent control in combatting PRV infections in Yunnan Province, China.

In order to explore the relationship between lung and intestinal injury and microorganisms in piglets caused by PRV infection.36 piglets were randomly divided into the blank group and the exposed group (or PRV group). PBS and PRV 1mL/Piggy were given by nasal drip at 0d, and the clinical symptoms were recorded every day. Three piglets in each group were sacrificed at 0d, 12h, 24h, 3d, 10d and 14d, respectively. The lungs, colon and contents were collected to observe the pathological sections and assess damage. The antigenic localization and expression of PRV, TLR4, NF-κB and MYD88 were detected by immunohistochemistry, the contents of sIgA, IFN-γ and IL-2 were determined by ELISA, and the microorganisms in lung and colon were analyzed by 16SrDNA. Accordingly, the correlation between lung and intestinal damage was highly significant (P<0.01). The expression of PRV in lung and colon was positively correlated with injury, with highly significant differences. The expression of TLR4, MYD88 and NF-κB was positively correlated with lung and intestinal injury. Besides, the levels of IFN-γ and sIgA were correlated with the injury, with significant differences. The species richness, diversity and evenness of microorganisms in lung and colon of the exposed group were reduced. There was a new Mycoplasma phylum in intestinal tract, and the correlation between lung flora and injury was higher than that in colon. In summary, it is evident that PRV infection with lung injury alters the intestinal TLR4-MYD88-NF-κB pathway, generating an inflammatory response, and lung and intestinal injury and microbial changes promote each other and drive disease progression.

The pseudorabies virus (PRV) is a highly neurotropic zoonotic pathogen. PRV infection can lead to neuroinflammation and damage to the blood-brain barrier (BBB). Elevated matrix metalloproteinase-9 (MMP-9) expression has a detrimental impairs BBB function. However, the source of elevated MMP-9 expression and function of MMP-9 in PRV invasion of the central nervous system (CNS), and the mechanism by which PRV breaches the BBB, remain poorly understood. This study explored the role of MMP-9 in the permeation of the BBB by PRV and clarified the molecular pathways involved in PRV invasion. In PRV-infected mice, severe neurological symptoms, perivascular cuffing, and an increase in the separation of membranes at the tight junctions were observed via electron microscopy. These results indicated that PRV infection destroys the BBB. Simultaneously, we discovered that the breakdown of the BBB that occurs in viral encephalopathy induced by PRV infection was attributable to the degradation of collagen IV mediated by MMP-9. Furthermore, we determined that astrocytes contributed to the increased levels of MMP-9. Using an in vitro double-layer Transwell BBB model, we found that PRV invades the CNS through a para-cellular pathway, triggering an "inflammatory storm.” These findings highlight the pivotal role of MMP-9 in PRV penetration of the BBB, enhance our understanding of the mechanisms underlying BBB disruption caused by PRV infection, and highlight potential targets for the development of preventive and therapeutic strategies against PRV infection.

The aim of the experiment was to investigate the antibacterial and anti-inflammatory effects of fermented flavones from the stem and leaf of Scutellaria baicalensis, Escherichia coli, Salmonella, Shigella, and Staphylococcus aureus were used as test strains, the MIC, MBC, and inhibitory circle size were determined. A total of 50 SPF grade Kunming mice were randomly divided into five groups with 10 mice in each group. Mice in all groups except the control group (Con group) were intraperitoneally injected with lipopolysaccharide (LPS, 4 mg/kg), and mice in the Con group were administrated with the same dose of normal saline. The positive drug group (LPS + DM group) was given 0.5 mg/kg dexamethasone. The original drug group (LPS + SBSL group) and fermentation drug group (LPS + FSBSL group) were fed the 8 mg/kg original drug and fermentation flavones. The experiment lasted for seven days. The results showed that the lowest MIC and MBC values of fermented flavones were Escherichia coli and Staphylococcus aureus, respectively. At 250 g/L, fermented flavones showed moderate sensitivity to Escherichia coli, Shigella, and Staphylococcus aureus. Compared with the LPS group, the mortality of mice in the LPS + FSBSL group was significantly reduced. The liver index in the LPS + SBSL group was extremely higher than that in the LPS + FSBSL group (P<0.01), and the spleen index in the LPS group was extremely higher than that in the Con group (P<0.01). Compared with the LPS group, the serum IL-6 content in the LPS + DM group and LPS + SBSL group was extremely increased (P<0.01). Compared with the LPS + DM group, the serum IL-6 content of mice in the LPS + SBSL group and LPS + FSBSL group was extremely increased (P<0.01). Compared with the Con group, the serum TNF-α content of mice in the LPS group was significantly increased (P<0.05). Compared with the LPS group, the content of IL-6 in the lung tissue of mice in the LPS + FSBSL group was significantly increased (P<0.05). Compared with the LPS + SBSL group, the content of IL-1β in the lung tissue of mice in the LPS + FSBSL group was significantly increased (P<0.05). The study indicates that fermented flavones from the stem and leaf of Scutellaria baicalensis have a good antibacterial effect on Shigella and Staphylococcus aureus, and the safe dose is 8 mg/kg, which significantly inhibite the mortality of mice infected with LPS, and affects the release of inflammatory factors IL-6, IL-1β, and TNF-α in the serum and lung of mice infected with LPS.

The objective of this study was to investigate the protective effect of Crataegus pinnatifida polysaccharide (CPP) on non-alcoholic fatty liver disease (NAFLD) induced by a high-fat diet (HFD) in mice. The findings demonstrated that CPP improved free fatty acid (FFA)-induced lipid accumulation in HepG2 cells and effectively reduced liver steatosis and epididymal fat weight in NAFLD mice, as well as decreased serum levels of TG, TC, AST, ALT, and LDL-C. Furthermore, CPP exhibited inhibitory effects on the expression of fatty acid synthesis genes FASN and ACC while activating the expression of fatty acid oxidation genes CPT1A and PPARα. Additionally, CPP reversed disturbances in intestinal microbiota composition caused by HFD consumption. CPP decreased the firmicutes/Bacteroidetes ratio, increased Akkermansia abundance, and elevated levels of total short-chain fatty acid (SCFA) content specifically butyric acid and acetic acid. Our results concluded that CPP may intervene in the development of NAFLD by regulating of intes-tinal microbiota imbalance and SCFAs production. Our study highlights that CPP has a potential to modulate lipid-related pathways via alterations to gut microbiome composition thereby ex-erting inhibitory effects on obesity and NAFLD development.

Pseudorabies virus (PRV) can cause fatal encephalitis in newborn pigs and escape the immune system. While there is currently no effective treatment for PRV, Scutellaria baicalensis Georgi polysaccharides (SGP) and Rodgersia sambucifolia Hemsl flavonoids (RHF) are traditional Chinese herbal medicines with potential preventive and therapeutic effects against PRV infection. In order to explore which one is more effective in the prevention and treatment of PRV infection in piglets. We investigate the therapeutic effects of RHF and SGP in PRV-infected piglets using clinical symptom and pathological injury scoring systems. The immune regulatory effects of RHF and SGP on T lymphocyte transformation rate, cytokines, T cells, and Toll-like receptors were also measured to examine the molecular mechanisms of these effects. The results showed that SGP significantly reduced clinical symptoms and pathological damage in the lungs, liver, spleen, and kidneys in PRV-infected piglets and the T lymphocyte conversion rate in the SGP group was significantly higher than that in the other treatment groups, this potential dose-dependent effect of SGP on T lymphocyte conversation. Serum immunoglobulin and cytokine levels in the SGP group fluctuated during the treatment period, with SGP treatment showing better therapeutic and immunomodulatory effects in PRV-infected piglets than RHF or the combined SGP + RHF treatment. In conclusion, RHF and SGP treatments alleviate the clinical symptoms of PRV infection in piglets, and the immunomodulatory effect of SGP treatment was better than that of the RHF and a combination of both treatments. This study provides evidence for SGP in controlling PRV infection in piglets.

Medicinal plants are considered a repository of bioactive ingredients. Rodgersia sambucifolia (Hemsl), a herbaceous perennial originating from East Asia, has demonstrated bacteriostatic and antiviral properties. The aim of this study was to identify an effective extraction procedure for isolating potential bacteriostatic and antiviral compounds from the plant. The crude extracts were obtained using ethanol, methanol or acetone, and stepwise extracted with ethyl acetate, n-butanol or water. The minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), and diameters of the inhibition zone were evaluated for bacteriostatic efficacy. These tests were carried out with Enterococcus faecalis, Enterococcus faecium, Shigella dysenteriae, Streptococcus lactis, Staphylococcus aureus, and Streptococcus lactis. The antiviral activities of prevention, treatment, and neutralization, utilizing pseudorabies virus, were evaluated using swine testicular cell viability. The active ingredients from the best bioactivity extraction procedure were analyzed using liquid chromatography-mass spectrometry (LC-MS). When ranked highest to lowest, the bacteriostatic and antiviral effects were obtained in the order of the crude extracts prepared from ethanol, methanol, and acetone. Bacteriostatic and antiviral effects were highest in the stepwise extraction of ethyl acetate, followed by the extraction of n-butanol and water. The main compounds identified by LC-MS in the ethyl acetate phase in descending order of content were: bergenin, palmitic acid, baicalein, linoleic acid, chrysin, γ-linolenic acid, catechin gallate, catechin, ursolic acid, and baicalin. This study provides a research basis for the development of bacteriostatic and antiviral drugs from traditional Chinese herbal medicines.