4.7 Article

Abietic acid ameliorates psoriasis -like inflammation and modulates gut microbiota in mice

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 272, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2021.113934

Keywords

Abietic acid; Gut microbiota; Psoriasis; Anti-inflammation

Funding

  1. Health Research Foundation Project of Shaanxi Province, China [2018E009]
  2. Research Foundation Project of Shaanxi Provincial Hospital of TCM, China [2018-16]

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Oral administration of abietic acid (AA) alleviated IMQ-induced psoriasis-like skin inflammation in mice by regulating Th17/Treg cell balance, reducing serum cytokine levels, and modulating gut microbiota composition. The study suggests that AA may be a potential candidate for treating psoriasis through inhibiting immune responses and influencing gut microbiota.
Ethnopharmacological relevance: Abietic acid (AA), an antibacterial terpenoid, was initially isolated from rosin which has been used as a traditional Chinese medicine to treat psoriasis. In our previous works, we found that water-processed rosin (WPR) can alleviate imiquimod (IMQ)-induced psoriasis-like inflammation in mice. However, the efficacy of AA, the main component of WPR, against psoriasis remains unclear. Materials and methods: In this study, we confirmed the anti-psoriasis efficacy of AA (40 mg/kg daily for 7 days) in IMQ-induced psoriasis-like inflammation BALB/c mouse model by the psoriasis area severity index (PASI), flow cytometry, ELISA, histopathological and immunohistochemical analysis. Furthermore, we detected the relative abundance of gut microbe using high-throughput 16S rRNA gene sequencing to validate whether AA modulate gut microbe. Result: Oral administration of AA ameliorates IMQ-induced psoriasis-like skin inflammation through reducing PASI scores, regulating the balance of Th17/Treg cells in the mouse spleen, and downregulating the level of serum cytokines such as TNF-alpha, IL-17A, TGF-1 beta, and IL-23. 16S rRNA gene sequencing revealed that the relative abundance of gut bacteria related to inflammation, such as, Anaerotruncus and Christensenella at genus level were decreased, while Kurthia, Citrobacter, and Klebsiella at genus level were increased in AA group mice. Additionally, the correlation analysis illustrated that the key microbiota had a close relationship with the psoriasis-like inflammation related indexes. Conclusion: AA might exert the anti-psoriasis effect via inhibiting Th17-related immune responses, hinting that it might be a candidate for treating psoriasis. Meanwhile, the alteration of intestinal microbiota by AA treatment is another possible explanation for the amelioration of imiquimod-induced psoriasis-like inflammation.

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