Lactobacillus rhamnosus CY12 Enhances Intestinal Barrier Function by Regulating Tight Junction Protein Expression, Oxidative Stress, and Inflammation Response in Lipopolysaccharide-Induced Caco-2 Cells

The intestinal barrier is vital for preventing inflammatory bowel disease (IBD). The objectives of this study were to assess whether the Lactobacillus rhamnosus CY12 could alleviate oxidative stress, inflammation, and the disruption of tight junction (TJ) barrier functions induced by lipopolysaccharide (LPS), and therefore to explore the potential underlying molecular mechanisms. Our results showed that LPS-induced Cancer coli-2 (Caco-2) cells significantly increased the levels of reactive oxygen species (ROS), lactate dehydrogenase, inflammatory cytokines interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor-alpha (IL-1 beta, IL-6, IL-8, and TNF-alpha), and the cell apoptosis rate while decreasing the levels of TJ proteins occludin, zonula occludens-1 (ZO-1), and claudin and antioxidant enzymes, such as catalase, superoxide dismutase, and glutathione peroxidase(CAT, SOD, and GSH-Px) (p < 0.05). However, Lactobacillus rhamnosus CY12 could relieve cytotoxicity, apoptosis, oxidative stress, and pro-inflammatory cytokine expressions, and also inhibit the Toll-like receptor 4/nuclear factor kappa-B(TLR4/NF-kappa B) signaling pathway. Furthermore, the gene expression of antioxidant enzymes, as well as the mRNA and protein expressions of TJ proteins, was improved. Particularly, the concentration of 10(8) cfu/mL significantly prevented the inflammatory injury induced by LPS in Caco-2 cells (p < 0.05). These findings support a potential application of Lactobacillus rhamnosus CY12 as a probiotic to prevent LPS-induced intestinal injury and treat intestinal barrier dysfunction.

Automated summary

In this study, Lactobacillus rhamnosus CY12 was found to alleviate oxidative stress, inflammation, and disruption of tight junction barrier functions induced by lipopolysaccharide. The protective effects were mediated through modulation of antioxidant enzyme gene expression, as well as mRNA and protein expressions of tight junction proteins, and inhibition of the TLR4/NF-κB signaling pathway.