Tissue & cell · 2026
Phenethylamine modulates intestinal inflammation and barrier integrity in diarrhea-predominant irritable bowel syndrome through the TAAR1-PKC signaling pathway.
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Cai Li, Chen Ping, Mou Weina, Zhang Lu, Li Xiaoliang, Xue Liwei
Аннотация
OBJECTIVE: This study investigated the role of phenethylamine (PEA) in diarrhea-predominant irritable bowel syndrome (IBS-D) and whether it induces intestinal barrier dysfunction and inflammation via the TAAR1-PKC pathway.
METHODS: An IBS-D mouse model was established, and PEA levels in the small intestine, colon, and serum were measured. Exogenous PEA was administered to assess its effects on stool water content, defecation frequency, and consistency. Western blotting evaluated tight junction proteins, inflammatory cytokines, and pathway proteins. The TAAR1 antagonist EPPTB was used to examine its ability to mitigate PEA-induced effects.
RESULTS: IBS-D mice showed elevated PEA levels in the colon and serum, correlating with aggravated diarrhea. Exogenous PEA increased stool water content and defecation frequency, worsened stool consistency, reduced barrier protein expression, and elevated inflammatory cytokines. PEA upregulated TAAR1, PKC, and CRF expression. EPPTB partially alleviated PEA-induced inflammation and barrier disruption but did not completely reverse these changes.
CONCLUSION: PEA contributes to IBS-D pathogenesis by promoting inflammation and impairing intestinal barrier function through TAAR1-PKC activation, potentially involving additional signaling mechanisms. These findings highlight the TAAR1-PKC pathway as a potential therapeutic target for IBS-D.
METHODS: An IBS-D mouse model was established, and PEA levels in the small intestine, colon, and serum were measured. Exogenous PEA was administered to assess its effects on stool water content, defecation frequency, and consistency. Western blotting evaluated tight junction proteins, inflammatory cytokines, and pathway proteins. The TAAR1 antagonist EPPTB was used to examine its ability to mitigate PEA-induced effects.
RESULTS: IBS-D mice showed elevated PEA levels in the colon and serum, correlating with aggravated diarrhea. Exogenous PEA increased stool water content and defecation frequency, worsened stool consistency, reduced barrier protein expression, and elevated inflammatory cytokines. PEA upregulated TAAR1, PKC, and CRF expression. EPPTB partially alleviated PEA-induced inflammation and barrier disruption but did not completely reverse these changes.
CONCLUSION: PEA contributes to IBS-D pathogenesis by promoting inflammation and impairing intestinal barrier function through TAAR1-PKC activation, potentially involving additional signaling mechanisms. These findings highlight the TAAR1-PKC pathway as a potential therapeutic target for IBS-D.