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

文献类型： 外文期刊

第一作者： Chen, Fengming

作者： Chen, Fengming;Wu, Shu;Wang, Xiaoyu;He, Binsheng;Fu, Yafen;Huang, Xingguo;Chen, Jiayi;Chen, Fengming;Li, Yinghui;Huang, Xingguo;Wu, Shu

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关键词： Oxidative stress; Lactobacillus delbrueckii; IPEC-J2; Intestinal injuries; TLRs

期刊名称：PROBIOTICS AND ANTIMICROBIAL PROTEINS （ 影响因子：4.4； 五年影响因子：5.0 ）

ISSN： 1867-1306

年卷期： 2025 年

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收录情况： SCI

摘要： 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 10(10) 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.

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