ArticleBulletin of experimental biology and medicine2026
Anti-Inflammatory Immunoregulatory Effects of Taurocholic Acid Are Mediated by TGR5.
Article in Bulletin of experimental biology and medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
TGR5 is a transmembrane protein that transmits the signals into intracellular space. In animals, taurocholic acid (TCA) is a natural bioactive substance in bile acid moiety regulating the TGR5-mediated anti-inflammatory immune response, which is a promising pharmacological target for treating some diseases associated with inflammation. Previously, we established that TCA-mediated immunoregulation could be implemented via modulation of expression of genes and proteins TNFα and IL-1β. In this study, we examined TGR5-mediated anti-inflammatory immune regulation by TCA. The anti-inflammatory signal transduction pathways triggered by TGR5 and the effects of TCA on TNFα and IL-1β were studied using ELISA, real-time quantitative PCR, immunofluorescence, and Western blotting. TCA specifically induced TGR5 internalization and upregulated production of cyclic AMP in a dose-dependent manner in HEK-293T cells transfected with TGR5. The effect of taurine-conjugated lithocholic acid (TLCA) on production of cyclic AMP was stronger than that of TCA in HEK-293T cells transfected with TGR5. LPS elevated expression of TNFα and IL-1β, but this proinflammatory effect was inhibited by TCA. A novel type of NR8383 cell line expressing human TGR5 (NR8383-TGR5 cells) was developed and tested. In NR8383 and NR8383-TGR5 cells, TGR5 increased expression of TNFα and IL-1β, but TCA inhibited expression of these cytokines and their mRNAs. Thus, the anti-inflammatory immune regulatory action of TCA is mediated via TGR5, which modulates expression of TNFα and IL-1β.
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