Sericin peptides alleviate dextran sulfate-induced ulcerative colitis symptoms by modulating the Th17 cell differentiation pathway in C57BL/6 mice
The bio-functional activities of sericin, a silk protein, have been explored across various fields, underscoring its potential therapeutic applications due to anti-inflammatory, antioxidant, and wound-healing effects. Sericin has also been shown to ameliorate ulcerative colitis (UC). While previous studies have noted the effects of intact sericin on ameliorating UC to some extent, there remains a significant gap in understanding the mechanism of action of small molecule sericin peptide (SRP). In this study, we explored the therapeutic efficacy of SRP in a dextran sulfate sodium (DSS)-induced mouse model of UC. Various oral doses of SRP were administered, and their effects were assessed through a range of physiological and biochemical parameters associated with UC. Our findings demonstrated that SRP effectively alleviated UC symptoms, as evidenced by improved physiological indices and reduced inflammatory markers. Additionally, transcriptomic and proteomic analyses revealed that the beneficial effects of SRP on UC were linked to the regulation of key biological pathways, particularly those involved in Th17 cell differentiation. To further validate our data, Western-blot, and immunofluorescence assays verified that SRP modulates Th17 cell differentiation, alleviating inflammation and maintaining homeostasis within the colonic vascular environment. Furthermore, SRP treatment was shown to protect colonic mucosal function, contributing to the overall improvement in UC symptoms. By regulating Th17 cell differentiation and modulating inflammatory pathways, SRP presents a promising approach to managing UC and enhancing mucosal health.
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