Aflatoxin B1 is a contaminant widely found in food and livestock feed, posing a major threat to human and animal health. Recently, much attention from the pharmaceutical and food industries has been focused on curcumin due to its strong antioxidant capacity. However, the therapeutic impacts and potential mechanisms of curcumin on kidney damage caused by AFB1 are still incomplete. In this study, AFB1 triggered renal injury in mice, as reflected by pathological changes and renal dysfunction. AFB1 induced renal oxidative stress and interfered with the Keap1–Nrf2 pathway and its downstream genes (CAT, SOD1, NQO1, GSS, GCLC, and GCLM), as manifested by elevated oxidative stress metabolites and reduced antioxidant enzymes activities. Additionally, AFB1 was found to increase apoptotic cells percentage in the kidney via the TUNEL assay, along with increased expression of Cyt-c, Bax, cleaved-Caspase-3, Caspase-9, and decreased expression of Bcl-2 at the transcriptional and protein levels; in contrast, for mice given curcumin, there was a significant reversal in kidney coefficient, biochemical parameters, pathological changes, and the expression of genes and proteins involved in oxidative stress and apoptosis. These results indicate that curcumin could antagonize oxidative stress and apoptosis to attenuate AFB1-induced kidney damage.

Aflatoxin B1 (AFB1) is a stable toxic metabolite threatening health of human and animal and widely contaminated animal feed and human food. This present study aimed to investigate the effects of dietary curcumin on ileum injury in ducks induced by AFB1 administration and explore its underlying mechanisms. Ducks (N = 450, one-day-old male) with a similar weight were randomly assigned to 3 groups, containing the control group, AFB1 group (60 μg AFB1 kg⁻¹ body weight) and curcumin (500 mg curcumin kg⁻¹ diet) + AFB1 group. AFB1 administration markedly increased the ileum damage, AFB1-DNA adducts in the plasma and oxidation stress and inflammation. Adding curcumin into diet protected the ileum against morphology damage induced by AFB1 administration, decreased AFB1-DNA adducts in the plasma and eliminated oxidation stress and inflammation in the ileum of ducks. Anti-oxidation and anti-inflammatory effects of curcumin could protect the ileum against acute damage via activating Nrf2-ARE signaling pathway and inhibiting NF-κB signaling pathway. Conclusively, curcumin was a dietary anti-oxidation and anti-inflammation agent via activating Nrf2-ARE signaling pathway and inhibiting NF-κB signaling pathway to protect ileum against acute damage induced by AFB1 administration.

Antibacterial peptides (APMs) are a new type of antibacterial substance. The relationship between their structure and function remains indistinct; in particular, there is a lack of a definitive and fixed template for designing new antimicrobial peptides. Previous studies have shown that porcine Protegrin-1 (PG-1) exhibits considerable antimicrobial activity and cytotoxicity. In this study, to reduce cytotoxicity and increase cell selectivity, we designed histidine-rich peptides based on the sequence template RR(XY)₂X^DPGX(YX)₂RR-NH₂, where X represents I, W, V, and F. The results showed that the peptides form more β-hairpin structures in a lipid-rich environment that mimics cell membranes. Among them, the antimicrobial peptide HV2 showed strong antibacterial activity against Gram-negative strains and almost no toxicity to normal cells. The results of our analysis of its antibacterial mechanism showed that peptide HV2 acts on the bacterial cell membrane to increase its permeability, resulting in cell membrane disruption and death. Furthermore, peptide HV2 inhibited bacterial movement in a concentration-dependent manner and had a more robust anti-inflammatory effect by inhibiting the production of TNF-α. In summary, peptide HV2 exhibits high bactericidal activity and cell selectivity, making it a promising candidate for future use as an antibiotic.

Antimicrobial peptides (AMPs) have attracted more attention for their potential candidates for new antibiotic drugs. As a novel identified cathelicidin AMP from duck, dCATH owns broad-spectrum antimicrobial activities but with a noticeable toxicity. To explore dCATH-derived AMPs with reduced cell toxicity and improved cell selectivity, a series of truncated and tryptophan-replaced peptides of dCATH were designed. Two truncated peptides containing one of the two tryptophan (Trp) residues at the positions of 4 and 17 (W4 and W17) of dCATH, dCATH(1–16) and dCATH(5–20), showed strong antibacterial activity, but didn’t show obvious hemolytic activity and cytotoxicity. The derived peptides not containing Trp didn’t possess obvious antimicrobial activity, and their hemolytic and cytotoxic effect was also diminished. Also as evidence by Trp fluorescence experiment that existence of W4 and W17 was crucially important to the antimicrobial activity, hemolysis and cytotoxicity of dCATH, and one of the two Trp residues was competent and necessary to retain its antimicrobial activity. Antibacterial mechanism analysis showed that dCATH(1–16) and dCATH(5–20) killed bacterial cells by increasing permeability and causing a loss of membrane integrity. dCATH(1–16) and dCATH(5–20) possessed insignificant inhibitory activity against levels of IL-6, TNF-α, and NO in RAW 264.7 cells treated with LPS. In vivo, intraperitoneal administration of the two peptides significantly decreased mortality and provided protection against LPS-induced inflammation in mice challenged with lethal dose of LPS. The two peptides, dCATH(1–16) and dCATH(5–20), which possessed high antibacterial activity and cell selectivity, may herald development prospects as new antibacterial agents in the future.