ArticleScientific reports2017
Pseudolaric acid B attenuates atopic dermatitis-like skin lesions by inhibiting interleukin-17-induced inflammation.
Article in Scientific reports, 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, 19 citations in OpenAlex.
- Pseudolaric Acid B Alleviates Non-alcoholic Fatty Liver Disease by Targeting PPARα to Regulate Lipid Metabolism and Promote Mitochondrial Biogenesis.Chinese journal of integrative medicine · 2025Article
- Exo-Selective Intramolecular (4+3) Cycloadditions to Trans-Fused Perhydroazulenes: An Asymmetric Formal Synthesis of (-)-Pseudolaric Acid B.Angewandte Chemie (International ed. in English) · 2025Article
- Atopic Dermatitis: The Relationship Between Immune Mediators and Skin Lipid Barrier.Clinical reviews in allergy & immunology · 2025Review
- Emerging Therapeutics in the Fight Against EV-D68: A Review of Current Strategies.Influenza and other respiratory viruses · 2024Review
- SNPs in microRNA seed region and impact of miR-375 in concurrent regulation of multiple lipid accumulation-related genes.Scientific reports · 2024Article
- Anti-Inflammatory Herbal Extracts and Their Drug Discovery Perspective in Atopic Dermatitis.Biomolecules & therapeutics · 2024Review
- Pseudolaric acid B ameliorates synovial inflammation and vessel formation by stabilizing PPARγ to inhibit NF-κB signalling pathway.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudolaric acid B (PB), isolated from the extract of the root bark of Pseudolarix kaempferi Gordon, has been used as a traditional remedy for the treatment of skin diseases. However, the information of PB on atopic dermatitis (AD) remains largely unknown. In the present study, oral administration with PB improved the severity scores of AD-like skin lesions dose-dependently in NC/Nga mice through reducing serum IgE, pro-inflammatory cytokines, and the infiltration of inflammatory cells. In addition, PB significantly attenuated the levels of IL-17 and IL-22, and the proportion of Th17 cells in NC/Nga mice, as well as decreased IL-17-induced inflammation in RAW264.7 cells. Moreover, PB inhibited the phosphorylation of IκBα and miR-155 expression both in NC/Nga mice and in IL-17-stimulated RAW264.7 cells, which could be reversed by GW9662, a specific antagonist for PPARγ. The incorporation of GW9662 reversed the inhibitory effect of PB on the RORγ-mediated activation of the Il17 promoter. Transfection with PPARγ luciferase reporter gene further demonstrated the enhancement of PB on PPARγ transactivation. These findings indicate that PB could ameliorate AD-like skin lesions by inhibiting IL-17-induced inflammation in a PPARγ-dependent manner, which would provide experimental evidence of PB for the therapeutic potential on AD and other inflammatory skin diseases.
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