What question did this study set out to answer?

To investigate the physiological role and molecular mechanisms of the membrane-bound bile acid receptor TGR5 (Gpbar1) in regulating hepatic inflammatory responses.

July 6, 2011HepatologyOpen Access

The G-Protein-coupled bile acid receptor, Gpbar1 (TGR5), negatively regulates hepatic inflammatory response through antagonizing nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) in mice

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To investigate the physiological role and molecular mechanisms of the membrane-bound bile acid receptor TGR5 (Gpbar1) in regulating hepatic inflammatory responses.
Assessed NF-κB signaling dynamics, including IκBα phosphorylation, p65 nuclear translocation, and β-arrestin2 interactions, using in vitro assays and anti-β-arrestin2 small interfering RNA.
Evaluated hepatic necrosis and inflammatory mediator expression in wild-type and TGR5-knockout mice challenged with lipopolysaccharide, with and without a TGR5 agonist.
TGR5 activation suppressed IκBα phosphorylation, p65 translocation, and NF-κB transcriptional activity by promoting an interaction between IκBα and β-arrestin2, an effect reversed by β-arrestin2 knockdown.
TGR5-knockout mice exhibited significantly more severe liver necrosis and inflammatory responses compared to wild-type mice following lipopolysaccharide challenge.
Agonist activation of TGR5 inhibited lipopolysaccharide-induced inflammatory mediator expression in wild-type mice, but showed no inhibitory effect in TGR5-knockout mice.

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Implication

Animal study demonstrates that activating bile acid receptor TGR5 curbs liver inflammation in mice, highlighting a promising therapeutic target for inflammatory liver diseases.

Cite This Study

Wang et al. (2011) studied this question.

synapsesocial.com/papers/6a1d192e28423f2ce504c672 https://doi.org/10.1002/hep.24525

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Implication

Animal study demonstrates that activating bile acid receptor TGR5 curbs liver inflammation in mice, highlighting a promising therapeutic target for inflammatory liver diseases.

The G-Protein-coupled bile acid receptor, Gpbar1 (TGR5), negatively regulates hepatic inflammatory response through antagonizing nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) in mice

Key Points

Discussion

Implication

Cite This Study

The G-Protein-coupled bile acid receptor, Gpbar1 (TGR5), negatively regulates hepatic inflammatory response through antagonizing nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) in mice

Key Points

Discussion

Implication

Cite This Study

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