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Updated: Sep 9, 2025
Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation
Published on: July 27, 2022
Sesamin ameliorates ulcerative colitis by modulating the DUSP1/ERK feedback loop and restoring gut microbiota
Shuxia Cao1, Xiangyu Guo1, Mengyuan Xin1
1Key Laboratory of Cellular Function and Pharmacology of Jilin Province, Yanbian University, Yanji 133002, China.
Background:
Sesamin (SSM), a plant-derived lignan, possesses anti-inflammatory and immunomodulatory effects. The pathogenesis of ulcerative colitis (UC) is complex and involves intestinal mucosal damage, inflammation, and dysbiosis of the gut microbiota. However, to date, the protective effects and therapeutic mechanisms of SSM in UC have hardly been investigated.
Purpose:
The purpose of the study was to investigate the protective effects and therapeutic mechanisms of SSM in UC.
Methods:
This study utilized a dextran sulfate sodium-induced mouse model of UC to investigate the therapeutic effects of SSM and its impact on gut microbiota using molecular biology techniques, including histological staining, western blotting, proteomics, molecular docking, 16S rRNA sequencing, and fecal microbiota transplantation.
Results:
SM significantly alleviated inflammation, repaired intestinal mucosal barrier, and improved gut microbiota structure in mice with UC (p < 0.05). Further studies revealed that SSM upregulated dual-specificity phosphatase 1 (DUSP1) by suppressing extracellular signal-regulated protein kinase (ERK) phosphorylation, whereas DUSP1 knockdown increased p-ERK levels (p < 0.05). Additionally, SSM regulated the distribution of gut microbiota by increasing the abundance of beneficial bacteria (such as Lactobacillus), reducing the abundance of opportunistic pathogens (such as Staphylococcus), and restoring gut microbiota homeostasis (p < 0.05).
Conclusion:
In summary, this is the first study to demonstrate that SSM exerts anti-inflammatory and intestinal barrier-restoring effects through modulating the DUSP1/ERK feedback loop and restoring gut microbiota homeostasis, thereby offering a novel therapeutic strategy for UC.
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