Loganin alleviates LPS-activated intestinal epithelial inflammation by regulating TLR4/NF-κB and JAK/STAT3 signaling pathways.

Inflammatory bowel disease (IBD) is a chronic, recurrent gastrointestinal inflammation that affects millions of people around the world. Loganin, an iridoid glycoside, has shown the anti-inflammatory effects. However, the effect of loganin on IBD and its underlying molecular mechanism are not clear. The present study aimed to investigate whether loganin could alleviate IBD and its mechanisms. The intestinal epithelial Caco-2 cell line was treated with lipopolysaccharide (LPS) to establish an in vitro IBD model. MTT assay was used to detect cell viability. The expression and release level of inflammatory factors were determined by both real-time-PCR and ELISA. Western blotting was used to assess the NF-kappa B and JAK/STAT3 pathway-related protein levels. The results showed that loganin repressed the expression and release of IL-6, TNF-alpha, and IL-1 beta, and inhibited TLR4/NF-kappa B and JAK/STAT3 signaling pathways in a concentration-dependent manner. Overexpression of TLR4 could reverse the effect of loganin, leading to activation of NF-kappa B signaling and production of inflammatory factors. Meanwhile, IGF-1, a JAK/STAT3 signaling activator, could also reverse the anti-inflammation effect of loganin. In conclusion, loganin inhibited LPS-activated intestinal epithelial inflammation by repressing TLR4/NF-kappa B and JAK/STAT3 signaling pathway.