The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), and an OTA+ASTA group (JG). Oxidative indices (malondialdehyde (MDA), total superoxide dismutase (T-SOD), and reduced glutathione (GSH)) and inflammatory markers (interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α)) were assayed in the lung, and the lung-weight-to-body-weight ratio was calculated. Apoptosis was detected in pathological sections by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Oxidative damage and inflammation were detected in the lung of mice after exposure to OTA. Besides, Nrf2- and NF-κB-pathway-associated proteins were detected by Western blot. In contrast with OTA, ASTA significantly raised the expression of Nrf2, HO-1, and MnSOD, while the expression of other proteins (Keap1, TLR4, and NF-κB) was significantly decreased. These results indicate that ASTA exerted protective effects against OTA-induced oxidative damage and inflammation in the lung by regulating the Nrf2 and NF-κB pathways.

Listeria monocytogenes is a foodborne pathogen that can cause listeriosis in humans and animals. It is of significant concern to the food industry as it can grow at low temperatures. Aggravatingly, only some of the commonly used food preservatives can effectively inhibit the growth of LM. In this study, the effectiveness of synthetic analogs of antimicrobial peptides from Limulus in inhibiting the growth of LM was studied. As determined by the Kirby–Bauer disc diffusion method, the diameters of the inhibition zones produced by the synthetic antimicrobial peptides ranged from 8.24 mm to 8.86 mm, and the minimum inhibitory concentrations (MICs) of the peptides ranged from 40 μg/mL to 160 μg/mL. At their MICs, initially, the synthetic antimicrobial peptides exhibited bacteriostatic effects on LM. They permeabilized the cell membrane of the bacterium and suppressed virulence genes (the inlA, prfA, and hly genes) in the bacterium. However, the bacteriostatic effects were effective only for 1 h, after which the bacterium slowly became resistant to them. After 6 h, the bacterium resumed its growth. Although cells in treatment groups resumed their growth after 6 h, the growth of the cells was inhibited compared to the growth of cells in the control group. Further studies are necessary to reduce the resistance of LM to the antibacterial effects of the synthetic antimicrobial peptides.