Adsorption of deoxynivalenol by APTS-TEOS modified eggshell powder.

Deoxynivalenol (DON) is widely contaminated in foods and feeds, which greatly threatens human and animal health. Due to its stable physicochemical properties, DON can be hardly eliminated by heating or ultraviolet radiation. In the present study, the biowaste eggshells were firstly modified into effective DON adsorbents, which are ATPS (triethoxysilane) + TEOS (aminopropyl triethoxysilane) modified 500 °C/700 °C-calcined eggshell powders under acetic/propionic acid-catalyzation (500-CSAE, 500-CSPE, 700-CSAE, 700-CSPE). The adsorption rates of DON on the raw eggshell powder, 500-CSAE, 500-CSPE, 700-CSAE, and 700-CSPE in acidity-adjusted buffer solution were 14.6%, 53.0%, 47.8%, 29.9%, and 31.2%, respectively. Characteristic analysis implied that the mesopore structures and enriched Si-OH groups in the modified eggshell powders are involved in DON adsorption. Besides, 500-CSAE, 500-CSPE, and 700-CSPE were verified to numerically alleviate the viability loss of IPEC-J2 cells caused by DON. In conclusion, the novel modified eggshell powders exhibit great application prospects for DON control in foods and feeds.

Allicin Improves Intestinal Epithelial Barrier Function and Prevents LPS-Induced Barrier Damages of Intestinal Epithelial Cell Monolayers.

Gut barrier disruption is the initial pathogenesis of various diseases. We previously reported that dietary allicin improves tight junction proteins in the endoplasmic reticulum stressed jejunum. However, whether the allicin benefits the gut barrier within mycotoxin or endotoxin exposure is unknown. In the present study, IPEC-J2 cell monolayers within or without deoxynivalenol (DON) or lipopolysaccharide (LPS) challenges were employed to investigate the effects of allicin on intestinal barrier function and explore the potential mechanisms. Results clarified that allicin at 2 µg/mL increased the viability, whereas the allicin higher than 10 µg/mL lowered the viability of IPEC-J2 cells via inhibiting cell proliferation. Besides, allicin increased trans-epithelial electric resistance (TEER), decreased paracellular permeability, and enhanced ZO-1 integrity of the IPEC-J2 cell monolayers. Finally, allicin supplementation prevented the LPS-induced barrier damages via activating Nrf2/HO-1 pathway-dependent antioxidant system. In conclusion, the present study strongly confirmed allicin as an effective nutrient to improve intestinal barrier function and prevent bacterial endotoxin-induced barrier damages.