Weanling stress and toxicosis, which are harmful to the health of pigs’ intestines, are associated with oxidative stress. Quercetin (Que) is a polyphenolic compound that shows good anti-cancer, anti-inflammation and anti-oxidation effects. This study aimed to elaborate whether or not Que promotes IPEC-J2 (intestinal porcine enterocyte cells) proliferation and protects IPEC-J2 from oxidative damage. Thus, we examined the effects of Que on proliferation and H₂O₂-induced apoptosis in IPEC-J2. The results showed that Que increased IPEC-J2 viabililty, propelled cells from G1 phase into S phase and down-regulated gene levels of P27 and P21, respectively. Besides, H₂O₂-induced cell damage was alleviated by Que after different exposure times, and Que depressed apoptosis rate, reactive oxygen species (ROS) level and percentage of G1 phase cells and elevated the percentage of cells in G2 phase and S phase and mitochondrial membrane potential (Δψm) after IPEC-J2 exposure to H₂O₂. Meanwhile, Que reduced the value of Bax/Bcl-2 in H₂O₂ exposed cells. In low-degree oxidative damage cells, lipid peroxidation product malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were increased. In turn, Que could reverse the change of MDA content and SOD activity in low-degree damage cells. Nevertheless, catalase (CAT) activity was not changed in IPEC-J2 incubated with Que under low-degree damage conditions. Interestingly, relative expressive levels of the proteins claudin-1 and occludin were not altered under low-degree damage conditions, but Que could improve claudin-1 and occludin levels, slightly. This research indicates that Que can be greatly beneficial for intestinal porcine enterocyte cell proliferation and it protects intestinal porcine enterocyte cells from oxidation-induced apoptosis, and could be used as a potential feed additive for porcine intestinal health against pathogenic factor-induced oxidative damages and apoptosis.

Fumonisins (Fums) are types of mycotoxin that widely contaminante feed material crops, and can trigger potential biological toxicities to humans and various animals. However, the toxicity of Fums on porcine blood vessels has not been fully explored. Fumonisin B₁ (FB₁) is the main component of Fums. Therefore, the aim of this study was to explore the effects of FB₁ on the oxidative stress and tight junctions of the pig iliac endothelial cells (PIECs) in vitro. The results showed that FB₁ reduced the viability of PIECs, increased the contents of lipid peroxidation product malondialdehyde (MDA), decreased the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thioredoxin reductase (TrxR), and decreased the level of glutathione (GSH). In addition, the barrier functions were destroyed, along with the down-regulations on Claudin 1, Occludin and ZO-1 and the increase of paracellular permeability. Thus, this research indicates that FB₁ facilitates oxidative stress and breaks barrier functions to damage pig iliac endothelium cells.

Fumonisin B₁ (FB₁), which is a mycotoxin produced by Fusarium moniliforme and Fusarium rotarum, has a number of toxic effects in animals. Moldy feed containing FB₁ can damage the intestine. In this study, we used intestinal porcine epithelial cells (IPEC-J2) as an in vitro model to explore the effects of FB₁ on cell cycle and apoptosis. The results showed that IPEC-J2 cells treated with 10, 20, and 40 μg/mL FB₁ for 48 h experienced different degrees of damage manifested as decreases in cell number and viability, as well as cell shrinkage and floating. In addition, FB₁ reduced cell proliferation and the mRNA and protein expression of proliferating cell nuclear antigen (PCNA), cyclin-dependent kinase 2 (CDK2), CDK4, cyclinD1, and cyclinE1. FB₁ blocked the cell cycle in the G1 phase. FB₁ also induced mitochondrial pathway apoptosis, reduced mitochondrial membrane potential, and promoted mRNA and protein expression of Caspase3, Caspase9, and Bax. The findings suggest that FB₁ can induce IPEC-J2 cell damage, block the cell cycle, and promote cell apoptosis.

The T-2 toxin is a frequent contaminant in the global environment and agricultural production. Existing evidence suggests that the ingested T-2 toxin can enter the brain and exhibit neurotoxicity. However, it is still unknown whether T-2 toxin causes the depression-like behaviors. In this study, the mice were orally administrated with 1.5 mg/kg T-2 toxin daily for 14 d, and the depression-like behaviors were assessed by the tail suspension test (TST) and sucrose preference test (SPT). Here, the results showed that T-2 toxin exposure induced depression-like behaviors, manifested as behavioral despair and anhedonia, without anxiety-like behaviors. In addition, the reduced dopamine (DA) level and elevated dopamine transporter (DAT) level were found in reward center nucleus accumbens (NAc) receiving DAergic projection from ventral tegmental area (VTA) in brain after T-2 toxin administration, while there was no significant alteration in DA synthesis-related tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) in VTA and DA storage-related vesicle monoamine transporter 2 (VMAT2) in NAc. The local administration of DAT inhibitor AHN 1-055 hydrochloride into NAc alleviated T-2 toxin caused the depression-like behaviors. Importantly, the chemogenetic activation of the VTA^DA-NAc circuit increased the DA content in NAc and reversed the T-2 toxin-produced behavioral despair and anhedonia. Thus, our study for the first time illustrates DA dysregulation by upregulated DAT in NAc mediates T-2 toxin-triggered depression-like symptoms in mice. Meanwhile, this study establishes a novel causal relation between the neurotoxicant T-2 toxin exposure and the etiology of depression-like behaviors, and provides reference for the prevention and treatment for mycotoxin-induced depression-like symptoms.