Aflatoxin B₁ (AFB₁), a threatening mycotoxin, usually provokes oxidative stress and causes hepatotoxicity in animals and humans. Luteolin (LUTN), well-known as an active phytochemical agent, acts as a strong antioxidant. This research was designed to investigate whether LUTN exerts protective effects against AFB₁-induced hepatotoxicity and explore the possible molecular mechanism in mice. A total of forty-eight mice were randomly allocated following four treatment groups (n = 12): Group 1, physiological saline (CON). Group 2, treated with 0.75 mg/kg BW aflatoxin B₁ (AFB₁). Group 3, treated with 50 mg/kg BW luteolin (LUTN), and Group 4, treated with 0.75 mg/kg BW aflatoxin B₁ + 50 mg/kg BW luteolin (AFB₁ + LUTN). Our findings revealed that LUTN treatment significantly alleviated growth retardation and rescued liver injury by relieving the pathological and serum biochemical alterations (ALT, AST, ALP, and GGT) under AFB₁ exposure. LUTN ameliorated AFB₁-induced oxidative stress by scavenging ROS and MDA accumulation and boosting the capacity of the antioxidant enzyme (CAT, T-SOD, GSH-Px and T-AOC). Moreover, LUTN treatment considerably attenuates the AFB₁-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression. Notably, administration of LUTN up-regulated the Nrf2 and its associated downstream molecules (HO-1, NQO1, GCLC, SOD1) at mRNA and protein levels under AFB₁ exposure. Our results indicated that LUTN effectively alleviated AFB₁-induced liver injury, and the underlying mechanisms were associated with the activation of the Nrf2 signaling pathway. Taken together, LUTN may serve as a potential mitigator against AFB₁-induced liver injury and could be helpful for the development of novel treatment to combat liver diseases in humans and/or animals.

Host defense peptides (HDPs) are efficient defense components of the innate immune system, playing critical roles in intestinal homeostasis and protection against pathogens. This study aims to investigate the interference effects of DON on the intestinal porcine HDPs expression in piglets and intestinal porcine epithelial cell line (IPEC-J2) cells, and elucidate the underlying mechanisms through which it functions. In an animal experiment, intestinal HDPs were determined in weaned piglets fed control and 1.28 mg/kg or 2.89 mg/kg DON-contaminated diets. Dietary exposure to DON significantly decreased piglet average daily gain, increased intestinal permeability and depressed the expression of porcine β-defensin1 (pBD1), pBD2, pBD3, epididymis protein 2 splicing variant C (pEP2C), PMAP23, and proline/arginine-rich peptide of 39 amino acids (PR39) in the intestine (p < 0.05). In IPEC-J2 cells, DON decreased cell viability and inhibited the expression of pBD1, pBD3, pEP2C, PG1-5, and PR39 (p < 0.05). NOD2, key regulator that is responsible for HDPs production, was markedly downregulated, whereas caspase-12 was activated in the presence of DON. In conclusion, DON induced caspase-12 activation and inhibited the NOD2-mediated HDPs production, which led to an impaired intestinal barrier integrity of weaned piglets. Our study provides a promising target for future therapeutic strategies to prevent the adverse effects of DON.

Zearalenone (ZEN) is one of the most common contaminating mycotoxins and is mainly produced by Fusarium graminearum. ZEN and its metabolites can interfere with estrogen function and affect animals' reproductive ability. Pigs are most susceptible to ZEN, and ZEN is less harmful to poultry than to pigs. The exact mechanism for the difference in susceptibility remains unclear. In this review, we summarized some possible reasons for the relative insensitivity of poultry to ZEN, such as the lower total amount of α-zearalenol (α-ZOL) and the α-ZOL-to-β-ZOL ratio which reduce the toxicity of ZEN to poultry. The faster hepatic and enteric circulation, and excretion capacity in poultry can excrete more ZEN and its metabolites. There are other possible factors such as the transformation of intestinal microorganisms, differences in hydroxysteroid dehydrogenases' activity, high estrogen levels, and low estrogen receptors affinity which can also cause poultry to be relatively insensitive to ZEN. In this review, we summarized the hazards, pollution status, metabolic pathways, and some measures to mitigate ZEN's harmfulness. Specifically, we discussed the possible mechanisms of low reproductive toxicity by ZEN in poultry.