Astilbin emulsion improves guinea pig lesions in a psoriasis-like model by suppressing IL-6 and IL-22 via p38 MAPK.

Astilbin has anti-inflammatory and immunoregulatory effects, and is frequently used in prescriptions treating psoriasis; however, the mechanism remains to be fully elucidated. In the present study, the effect of an astilbin microemulsion on a psoriasis‑like model in guinea pigs was examined, and the underlying mechanism was investigated. The levels of interkeukin (IL)‑6, IL‑17A and IL‑22 were determined using fluorescent reverse transcription‑quantitative polymerase chain reaction analysis and enzyme‑linked immunosorbent assays. The phosphorylation of p38 and extracellular signal‑regulated kinase (ERK)1/2 was detected using western blot analysis. Compared with the untreated control, astilbin significantly ameliorated the lesions induced by propranolol hydrochloride. The effect of astilbin on cytokine levels were cytokine‑ and drug‑concentration‑dependent. At a concentration of 2.22 µM, astilbin decreased the mRNA expression levels of IL‑6, IL‑17A and IL‑22 in lipopolysaccharide (LPS)‑induced HaCaT cells by 89, 69.1 and 69.3%, respectively. However, 2.22 µM astilbin had no effect on the protein expression of IL‑17A, and decreased the protein expression levels of IL‑6 and IL‑22 by 79.2 and 49.5%, respectively (P<0.05). At a concentration of 11.10 µM, astilbin decreased the mRNA expression of IL‑6, which was significantly induced by LPS, and significantly (P<0.05) decreased the protein expression levels of IL‑6 and IL‑22. Additionally, astilbin inhibited the LPS‑induced activation of phosphorylated p38. These results suggested that astilbin has the potential to be developed into a topical drug for the treatment of psoriasis via the inhibition of inflammatory cytokines.