Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway

The aim of this study was to investigate the effect of luteolin (Lu) on dextran sodium sulfate (DSS)-induced colitis in mice. Mice spleen was weighed. The length of colon was measured. H&E staining was used to observe the pathological changes of colon in mice. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and intestine of mice were detected by commercial kits. Serum and intestinal cytokines were detected by ELISA kits. The expression of HMGB 1 mRNA was detected by real-time PCR. The expression of HMGB1-TLR-NF-kappa B pathway was detected by Western blot. The level of HMGB1 was detected by immunohistochemistry. The results showed that Lu significantly increased the colon length/body weight ratio and significantly decreased the spleen weight/body weight ratio. Lu significantly increased serum and intestinal SOD levels and decreased MDA levels. Lu significantly increased serum and intestinal cytokine levels in mice. qPCR and immunohistochemistry results showed that Lu significantly reduced HMGB1 mRNA level and protein level. In addition, Lu significantly reduced the expression of HMGB1-TLR-NF-kappa B signaling pathway protein of intestine in mice. In conclusion, Lu significantly reduced and alleviated DSS-induced colitis in mice, and the mechanism was related to the regulation of intestinal HMGB1-TLR-NF-kappa B signaling pathway in mice.

Automated summary

The study demonstrated that luteolin effectively improved colon health indicators and reduced inflammation levels in the affected areas by regulating the signaling pathways in the intestine to alleviate colitis.