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Aflatoxin B1 (AFB1) is a highly toxic secondary metabolite produced by Aspergillus species. Its extensive contamination of animal feed and human food poses significant health hazards to livestock and humans, with hepatotoxicity being a primary concern. This study investigated the protective effect of baicalin on AFB1-induced liver injury in ducklings. In the first experiment, ducklings were administered AFB1 at doses of 0, 6, 12, or 24 μg/kg body weight/day for 7 days to identify the optimal concentration for establishing a model of AFB1-induced growth performance and liver injury. Administration of AFB1, particularly at the higher doses (12 and 24 μg/kg body weight/day), significantly reduced growth performance and induced structural and functional liver injury (p < 0.05). In a second experiment, ducklings were administered AFB1 (12 μg/kg body weight/day) with or without baicalin (25–100 mg/kg body weight/day) for 7 days. Dietary baicalin significantly increased the serum albumin level; reduced the serum alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase levels; improved growth performance; and ameliorated structural and functional liver injury in ducklings exposed to AFB1 (p < 0.05). The results indicate that dietary baicalin alleviates AFB1-induced liver injury and growth performance decline in ducklings. Hence, baicalin could serve as a potential feed additive to reduce the harmful effects of AFB1 in the poultry breeding industry.

Through structure-based virtual screening, this study identified the botanical compound fangchinoline (FAN) as an inhibitor of the porcine aminopeptidase N (pAPN) receptor and evaluated its anti-transmissible gastroenteritis virus (TGEV) activity, mechanism, and safety. FAN exhibited potent antiviral efficacy against TGEV in PK-15 and IPEC-J2 cells (EC 50  = 2.862 μM and 3.670 μM, respectively), significantly reducing viral RNA copies and N protein expression while suppressing the upregulation of the inflammatory cytokines IL-6 and TNF-α. It also showed broad-spectrum potential by inhibiting PEDV (EC 50  = 2.243 μM). Mechanistic studies using a cellular thermal shift assay (CETSA) and drug affinity-responsive target stability (DARTS) confirmed that FAN can bind to pAPN, affecting its thermal and enzyme stability. Time-of-addition assays indicated that FAN interferes with both the early (attachment and internalization) and late replication phases of TGEV. In acute toxicity tests, FAN showed low toxicity (LD 50 in mice: 2060.23 mg/kg for males, 1481.93 mg/kg for females) and no mutagenic potential in the Ames test. Favorable pharmacokinetic parameters were also observed in rats. In conclusion, FAN exerts its anti-TGEV effect by targeting the critical pAPN receptor. Its plant origin, potent and broad-spectrum antiviral activity, elucidated mechanism, and promising safety profile support its further development as a lead compound for anti-coronavirus strategies.

At present, the treatment and prevention of infections in pigs mainly rely on antibiotics and vaccines, but inflammatory injury cannot be eliminated. The compound 18β-glycyrrhetinic acid (GA), a pentacyclic triterpenoid extracted from . root (liquorice) and with a chemical structure similar to that of steroidal hormones, has become a research focus because of its anti-inflammatory, antiulcer, antimicrobial, antioxidant, immunomodulatory, hepatoprotective and neuroprotective effects, but its potential for the treatment of vascular endothelial inflammatory injury by infections has not been evaluated. This study aimed to investigate the effects and mechanisms of GA intervention in the treatment of vascular endothelial inflammatory injury by infections. Putative targets of GA intervention in the treatment of vascular endothelial inflammatory injury by infections were identified using network pharmacological screening and molecular docking simulation. The cell viability of PIEC cells was investigated via the CCK-8 assay. The mechanism of GA intervention in the treatment of vascular endothelial inflammatory injury by infections were investigated using cell transfection and western blot. Through network pharmacological screening and molecular docking simulation, this study found that PARP1 may be a core target for GA to exert anti-inflammatory effects. Mechanistically, GA alleviates -induced vascular endothelial inflammation by PARP1-mediated NF-κB and HMGB1 signalling suppression. These findings, for the first time, demonstrate the potential therapeutic relationship among GA, PARP1 and inflammatory injury, providing a candidate drug, therapeutic targets and explanation for treating vascular endothelial inflammatory injury caused by infection.

Aflatoxin B 1 (AFB 1 ) is classified as a Class I carcinogen and common pollutant in human and animal food products. Prolonged exposure to AFB 1 can induce hepatocyte apoptosis and lead to hepatotoxicity. Therefore, preventing AFB 1 -induced hepatotoxicity remains a critical issue and is of great significance. Baicalin, a polyphenolic compound derived from Scutellaria baicalensis Georgi , has a variety of pharmacodynamic activities, such as antiapoptotic and anticancer activities. This study systematically investigated the alleviating effect of baicalin on AFB 1 -induced hepatotoxicity from the perspective of apoptosis and explored the possible molecular mechanism. In the normal human liver cell line L02, baicalin treatment significantly inhibited AFB 1 -induced c-Jun-N-terminal Kinase (JNK) activation and cell apoptosis. In addition, the in vitro mechanism study demonstrated that baicalin alleviates AFB 1 -induced hepatocyte apoptosis through suppressing the translocation of phosphorylated JNK to the nucleus and decreasing the phosphorylated c-Jun/c-Jun ratio and the Bax/Bcl2 ratio. Molecular docking and drug affinity responsive target stability assays demonstrated that baicalin has the potential to target JNK. This study provides a basis for the therapeutic effect of baicalin on hepatocyte apoptosis caused by AFB 1 , indicating that the development of baicalin and JNK pathway inhibitors has broad application prospects in the prevention of hepatotoxicity, especially hepatocyte apoptosis.

Aflatoxin B (AFB ) is classified as a Class I carcinogen and common pollutant in human and animal food products. Prolonged exposure to AFB can induce hepatocyte apoptosis and lead to hepatotoxicity. Therefore, preventing AFB -induced hepatotoxicity remains a critical issue and is of great significance. Baicalin, a polyphenolic compound derived from Scutellaria baicalensis Georgi, has a variety of pharmacodynamic activities, such as antiapoptotic and anticancer activities. This study systematically investigated the alleviating effect of baicalin on AFB -induced hepatotoxicity from the perspective of apoptosis and explored the possible molecular mechanism. In the normal human liver cell line L02, baicalin treatment significantly inhibited AFB -induced c-Jun-N-terminal Kinase (JNK) activation and cell apoptosis. In addition, the in vitro mechanism study demonstrated that baicalin alleviates AFB -induced hepatocyte apoptosis through suppressing the translocation of phosphorylated JNK to the nucleus and decreasing the phosphorylated c-Jun/c-Jun ratio and the Bax/Bcl2 ratio. Molecular docking and drug affinity responsive target stability assays demonstrated that baicalin has the potential to target JNK. This study provides a basis for the therapeutic effect of baicalin on hepatocyte apoptosis caused by AFB , indicating that the development of baicalin and JNK pathway inhibitors has broad application prospects in the prevention of hepatotoxicity, especially hepatocyte apoptosis.

Background: At present, the treatment and prevention of Pasteurella multocida infections in pigs mainly rely on antibiotics and vaccines, but inflammatory injury cannot be eliminated. The compound 18[beta]- glycyrrhetinic acid (GA), a pentacyclic triterpenoid extracted from Glycyrrhiza glabra L. root (liquorice) and with a chemical structure similar to that of steroidal hormones, has become a research focus because of its anti-inflammatory, antiulcer, antimicrobial, antioxidant, immunomodulatory, hepatoprotective and neuroprotective effects, but its potential for the treatment of vascular endothelial inflammatory injury by P. multocida infections has not been evaluated. This study aimed to investigate the effects and mechanisms of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections. Materials and Methods: Putative targets of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were identified using network pharmacological screening and molecular docking simulation. The cell viability of PIEC cells was investigated via the CCK-8 assay. The mechanism of GA intervention in the treatment of vascular endothelial inflammatory injury by P. multocida infections were investigated using cell transfection and western blot. Results: Through network pharmacological screening and molecular docking simulation, this study found that PARP1 may be a core target for GA to exert anti-inflammatory effects. Mechanistically, GA alleviates P. multocida-induced vascular endothelial inflammation by PARPl-mediated NF-[kappa]B and HMGB1 signalling suppression. Conclusion: These findings, for the first time, demonstrate the potential therapeutic relationship among GA, PARP1 and inflammatory injury, providing a candidate drug, therapeutic targets and explanation for treating vascular endothelial inflammatory injury caused by P. multocida infection. Keywords: network pharmacology, GA, PARP1, inflammatory injury, P. multocida infection

Background Simultaneous wastewater treatment and lipid production by oleaginous microalgae show great potential to alleviate energy shortage and environmental pollution, because they exhibit tremendous advantages over traditional activated sludge. Currently, most research on wastewater treatment by microalgal are carried out at optimized temperature conditions (25-35 °C), but no information about simultaneous wastewater treatment and lipid production by microalgae at low temperatures has been reported. Microalgal growth and metabolism will be inhibited at low temperature conditions, and satisfactory wastewater treatment performance will be not obtained. Therefore, it is critical to domesticate and screen superior microalgal strains with low temperature adaptability, which is of great importance for wastewater treatment and biodiesel production. Results In this work, simultaneous wastewater treatment and lipid production were achieved by a microalgal mutant Scenedesmus sp. Z-4 at the low temperature conditions (4, 10, and 15 °C). The results showed that algal growth was inhibited at 4, 10, and 15 °C compared to that at the optimal temperature of 25 °C. However, decreased temperature had no significant effect on the total cellular lipid content of algae. Importantly, lipid productivity at 10 °C was compromised by more net energy output relevant to biodiesel production, which demonstrated that the low temperature of 10 °C was favorable to wastewater treatment and energy recovery by Scenedesmus sp. Z-4. When molasses wastewater with optimal COD concentration of 8000 mg L−1, initial inoculation ratio of 15%, and C/N ratio of 15 was used to cultivate microalgae, the maximum removal rate of COD, TN, and TP at 10 °C reached 87.2, 90.5, and 88.6%, respectively. In addition, lipid content of 28.9% and lipid productivity of 94.4 mg L−1 day−1 were obtained. Conclusions Scenedesmus sp. Z-4 had good adaptability to low temperature conditions, and showed great potential to realize simultaneous wastewater treatment and lipid production at low temperatures. The proposed approach in the study was simple compared to other wastewater treatment methods, and this potential novel process was still efficient to remove COD, N, and P at low temperatures. Thus, it had a vital significance for the wastewater treatment in low temperature regions.

Wearable sensors have attracted considerable interest due to their ability to detect a variety of information generated by human physiological activities through physical and chemical means. The performance of wearable sensors is limited by their stability, and endowing wearable sensors with superhydrophobicity is one of the means to enable them to maintain excellent performance in harsh environments. This review emphasizes the imperative progress in flexible superhydrophobic sensors for wearable devices. Besides, the wettability principle and the mechanism of wearable sensors are briefly introduced to propose the combination of superhydrophobicity and wearable sensors. Next, superhydrophobic substrates for wearable sensors, including but not limited to, polydimethylsiloxane, polyurethane, gel, rubber, and fabric, are described in depth, and also the respective fabrication processes and performances. Moreover, the utility of superhydrophobic wearable sensors in a normal intelligent environment is described, highlighting their application in monitoring physiological signals, such as physical movement, pulse, vibration, temperature, perspiration, respiration, and so on. Finally, this review evaluates the challenges and dilemmas that wearable sensors must be overcome for further development and improve the functional performance of wearable sensors, paving the way for their expansion into advanced wearable sensing systems.

Insecticidal crystal toxins derived from the soil bacterium Bacillus thuringiensis (Bt) are widely used as biopesticide sprays or expressed in transgenic crops to control insect pests. However, large-scale use of Bt has led to field-evolved resistance in several lepidopteran pests. Resistance to Bt Cry1Ac toxin in the diamondback moth, Plutella xylostella (L.), was previously mapped to a multigenic resistance locus (BtR-1). Here, we assembled the 3.15 Mb BtR-1 locus and found high-level resistance to Cry1Ac and Bt biopesticide in four independent P. xylostella strains were all associated with differential expression of a midgut membrane-bound alkaline phosphatase (ALP) outside this locus and a suite of ATP-binding cassette transporter subfamily C (ABCC) genes inside this locus. The interplay between these resistance genes is controlled by a previously uncharacterized trans-regulatory mechanism via the mitogen-activated protein kinase (MAPK) signaling pathway. Molecular, biochemical, and functional analyses have established ALP as a functional Cry1Ac receptor. Phenotypic association experiments revealed that the recessive Cry1Ac resistance was tightly linked to down-regulation of ALP, ABCC2 and ABCC3, whereas it was not linked to up-regulation of ABCC1. Silencing of ABCC2 and ABCC3 in susceptible larvae reduced their susceptibility to Cry1Ac but did not affect the expression of ALP, whereas suppression of MAP4K4, a constitutively transcriptionally-activated MAPK upstream gene within the BtR-1 locus, led to a transient recovery of gene expression thereby restoring the susceptibility in resistant larvae. These results highlight a crucial role for ALP and ABCC genes in field-evolved resistance to Cry1Ac and reveal a novel trans-regulatory signaling mechanism responsible for modulating the expression of these pivotal genes in P. xylostella.

This randomized controlled trial aimed to compare the effects of butorphanol and sufentanil on early post-operative cognitive dysfunction (POCD) and systemic inflammation in older surgical patients. Patients (aged 65 years or above) undergoing surgeries with general anesthesia were randomized to either the butorphanol group (40 μg/kg during anesthesia induction) or the sufentanil group (0.4 μg/kg). Cognitive function changes during the perioperative period were assessed using the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA) scale up to 3 days after surgery. POCD was defined as a -score or composite -score greater than 1.96 for both MMSE and MoCA scores. Circulating inflammatory factors, including tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), and interleukin 10 (IL-10), were measured using enzyme-linked immunosorbent assay. The study included 114 patients (median age: 71 years, 57.7% male). Compared to sufentanil, butorphanol significantly reduced the incidence of POCD on the first (11.5% versus 32.7%,  = 0.017) and third day (3.8% versus 15.4%,  = 0.046) after surgery. Additionally, patients receiving butorphanol had significantly lower circulating levels of TNF-α and IL-1β at the time of discharge from the post-anesthesia care unit and on the first and third day after surgery (  < 0.05 for all comparisons). Furthermore, circulating IL-10 levels were significantly higher in patients receiving butorphanol (  < 0.05 for all comparisons). Administration of butorphanol during anesthesia induction, as opposed to sufentanil, was associated with a significant reduction in the early incidence of POCD in older surgical patients, possibly attributed to its impact on systemic inflammation. The present study was registered in the China Clinical Trial Center (ChiCTR2300070805, 24/04/2023).