ArticlePsychopharmacology2021
Ursolic acid ameliorates Nthy-ori 3-1 cells injury induced by IL-1β through limiting MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway.
Article in Psychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Lactoferrin alleviates oxidative stress and endoplasmic reticulum stress induced by autoimmune thyroiditis by modulating the mTOR pathway in the thyroid.Journal of endocrinological investigation · 2025Article
- Elucidating the molecular mechanisms underlying anti-inflammatory effects of Morchella esculenta in the arachidonic acid metabolic pathway by network pharmacology and molecular docking.Scientific reports · 2023Article
- Phytobioactive compounds as therapeutic agents for human diseases: A review.Food science & nutrition · 2023Review
- Recent Advances Regarding the Molecular Mechanisms of Triterpenic Acids: A Review (Part I).International journal of molecular sciences · 2022Review
- LncRNA MALAT1 Promotes PPARα/CD36-Mediated Hepatic Lipogenesis in Nonalcoholic Fatty Liver Disease by Modulating miR-206/ARNT Axis.Frontiers in bioengineering and biotechnology · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
rationaleUrsolic acid (UA) has exhibited anti-inflammatory and anti-oxidative drug effects.
objectivesIn the research, we assessed the effects of UA on Nthy-ori 3-1 cells stimulated by IL-1β and attempted to elucidate the mechanisms underlying the effects.
methodsAutoimmune thyroiditis (AIT) was simulated using Nthy-ori 3-1 cells by IL-1β (10 μM) treatment. UA (20 μM) was applied to ameliorate the injury of Nthy-ori 3-1 cells. The target of UA was predicted by TCMSP, BATMAN, and GEO database. Targeted relationship between lncRNA MALAT1 and miR-206, as well as miR-206 and PTGS1, was predicted by bioinformatics software and identified by dual luciferase assays. Cytokines in the cell supernatant and the apoptosis of cells were detected by ELISAs and flow cytometry assays, respectively. Expression levels of NF-κB signaling pathway-related proteins were estimated by western blot.
resultsBy enquiring TCMSP, BATMAN, and GEO database, PTGS1 was identified as a target of UA. Afterward, a ceRNA network among MALAT1, miR-206, and PTGS1 was constructed. The expression levels of MALAT1 and PTGS1 in AIT tissues were obviously enhanced. Moreover, the ceRNA network formed by MALAT1/miR-206/PTGS1 contributed to the damage of Nthy-ori 3-1 cells induced by IL-1β. However, UA ameliorated the Nthy-ori 3-1 cells injury induced by IL-1β through mediating the MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway.
conclusionsUA treatment significantly relieved the injury of Nthy-ori 3-1 cells via inhibiting the ceRNA mechanism of MALAT1/miR-206/PTGS1 and inflammatory pathways, insinuating that UA may be helpful for the treatment of AIT.
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