ArticleInternational journal of clinical and experimental pathology2017
Obeticholic acid improves hepatic steatosis and inflammation by inhibiting NLRP3 inflammasome activation.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Primary biliary cholangitis. Treatment options in 2025. A narrative review.Frontiers in immunology · 2025Review
- The role of botanical triterpenoids and steroids in bile acid metabolism, transport, and signaling: Pharmacological and toxicological implications.Acta pharmaceutica Sinica. B · 2024Review
- The adiponectin-derived peptide ALY688 protects against the development of metabolic dysfunction-associated steatohepatitis.Clinical and translational science · 2024Article
- Pyroptosis and gasdermins-Emerging insights and therapeutic opportunities in metabolic dysfunction-associated steatohepatitis.Frontiers in cell and developmental biology · 2023Review
- Role of the Inflammasome in Liver Disease.Annual review of pathology · 2022Review
- Article
- A Selective Adenosine AIn vivo (Athens, Greece)Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimSeveral pre-clinical and clinical researches have proved that obeticholic acid (OCA)has a potential therapeutic effect on non-alcoholic steatohepatitis (NASH). Our aim was to investigate whether the therapeutic effect of OCA on NASH was attributed to its inhibition effect on cytosolic sensor NLR family pyrin domain containing 3 (NLRP3) inflammasome activation.
methodsWe used mice model of methionine-choline-deficient (MCD) diet induced NASH. At different fibrosis stages, the expressions of NLRP3, caspase-1 and IL-1β were analyzed by means of immunohistochemistry and western blot respectively. After daily gavage of 0.4 mg of OCA or vehicle for 24 days, we evaluated the direct effect of OCA on NLRP3 inflammasome activation by analyzing the expressions of NLRP3 and IL-1β. Additionally, liver function and liver histology of mice were assessed. The expressions of NLRP3 and IL-1β above and the expressions of fibrosis-related genes were analyzed by quantitative real-time polymerase chain reaction (PCR).
resultsNLRP3 inflammasome activation could be observed in liver fibrosis, and we found that the expressions of NLRP3, caspase-1 and IL-1β gradually increased to peak at stage 2-3 but decreased significantly at stage 4 of liver fibrosis in MCD mice model. We also found that short-term OCA treatment could significantly down-regulate the expressions of NLRP3 and IL-1β and therefore improved NASH-associated steatosis and inflammation.
conclusionsNLRP3 inflammasome could be activated and might have an essential role in NASH progression, and short-term OCA treatment could have a potential therapeutic effect on NASH-associated steatosis and inflammation by inhibiting NLRP3 inflammasome activation.
Indexed as
Identifiers
31966664PMC6965461W3007318055What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.