Lactobacillus delbrueckii Alleviate Oxidative Stress and Intestinal Injuries by Activating TLR2 and TLR4 Expressions in IPEC-J2 Cells.

Abstract

Reducing the negative impact of oxidative stress (OS) on weaned piglets is crucial for the further development of the pig industry. Our previous studies found that Lactobacillus delbrueckii (LAB) can alleviate OS and protect intestinal health by activating TLR2 and TLR4 expressions in weaned piglets. This research aimed to verify whether LAB can alleviate OS and intestinal barrier injuries in IPEC-J2 cells by activating TLR2 and TLR4. IPEC-J2 cells were first pretreated with 10¹⁰ CFU/mL LAB for 12 h, and then were induced to OS by 0.8 mmol/L H₂O₂ for another 12 h. The results showed that LAB significantly alleviated OS induced by H₂O₂, indicated by the downregulation of MDA (P < 0.05), along with upregulation of GSH-Px, CAT, T-SOD, and T-AOC (P < 0.05). Besides, LAB significantly alleviated intestinal barrier injuries induced by H₂O₂, indicated by the upregulation of Claudin-1, Occludin, and ZO-1 expressions. Subsequently, the IPEC-J2 cells were pretreated with inhibitors of TLR2 (TLR2-IN-C29) and TLR4 (MD2-TLR4-IN-1) in the absence of LAB for 12 h, and then treated with 0.8 mmol/L H₂O₂ for another 12 h. The results showed that both inhibitors significantly prevented the protection effects of LAB on H₂O₂-induced OS, indicated by the downregulation of CAT, SOD1, HO-1, and GSH-Px1 expressions (P < 0.05). Taken together, LAB treatment can alleviate OS and intestinal injuries induced by H₂O₂ by activating TLR2 and TLR4 expressions in IPEC-J2 cells, thus providing novel theoretical support for LAB in the prevention and treatment of oxidative damage.