ArticleBioengineered2022
Peptide YY 3-36 attenuates trinitrobenzene sulfonic acid-induced colitis in mice by modulating Th1/Th2 differentiation.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- A Combined Colon Organoid-Sensory Neuron Model Reveals Epithelial Contribution to Moringin Efficacy Against Painful Inflammatory Bowel Disease.Phytotherapy research : PTR · 2026Article
- Gut Hormones and Inflammatory Bowel Disease.Biomolecules · 2025Review
- Antimicrobial Neuropeptides and Their Receptors: Immunoregulator and Therapeutic Targets for Immune Disorders.Molecules (Basel, Switzerland) · 2025Review
- Involvement of Intestinal Enteroendocrine Cells in Neurological and Psychiatric Disorders.Biomedicines · 2022Review
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Peptide YY (PYY) 3-36, the main circulatory form of PYY, plays important roles in gastrointestinal motility, secretion, and absorption. However, it is unknown whether PYY 3-36 has underlying functions in colitis. The Crohn's disease (CD)-like mouse model in which CD is induced by trinitrobenzene sulfonic acid (TNBS) was established and utilized to investigate this potential role for PYY 3-36. The results showed that the expression of colonic mucosal PYY and PYY receptors Y1, Y2, Y4 were significantly increased in mice with TNBS-induced colitis. In vitro, PYY 3-36 remarkably inhibited the production of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) from lipopolysaccharide (LPS)-induced macrophages. In vivo, a high concentration of PYY 3-36 robustly decreased the weight loss and death rate and attenuated the pathological colon tissue damage observed in mice with TNBS-induced colitis. Further studies uncovered that PYY 3-36 treatment reduced the levels of colon myeloperoxidase (MPO) and both colonic and systemic TNF-α and IL-6 observed in murine colitis. Furthermore, flow cytometric analysis showed PYY 3-36 altered the proportion of Th1/Th2 splenocytes in the disease model of colitis. Collectively, these results suggest that PYY 3-36 may be a promising candidate for the improvement of colitis, reflected by the attenuation of colon inflammatory responses observed in experimental murine colitis.
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