Cang-ai volatile oil ameliorates imiquimod-induced psoriatic skin lesions by suppressing the ILC3s

J Ethnopharmacol. 2024 May 23:326:117867. doi: 10.1016/j.jep.2024.117867. Epub 2024 Feb 10.

Abstract

Ethnopharmacological relevance: Cang-ai volatile oil (CAVO) is an aromatic Chinese medicine with potent antibacterial and immune regulatory properties. While CAVO has been used to treat upper respiratory tract infections, depression, otomycosis, and bacterial infections in the skin, its effect on psoriasis is unknown.

Aim of the study: This study explores the effect and mechanism of CAVO in psoriasis intervention.

Material and methods: The effect of CAVO on the expression of IL-6 and IL-1β was assessed in TNF-α-induced HaCaT cells using enzyme-linked immunosorbent assay (ELISA). Mice were given imiquimod (IMQ) and administered orally with different CAVO doses (0.03 and 0.06 g/kg) for 5 days. The levels of inflammatory cytokines related to group-3 innate lymphoid cells (ILC3s) in the skin were assessed using hematoxylin and eosin (H&E) staining, ELISA, and western blotting (WB). The frequency of ILC3s in mice splenocytes and skin cells was evaluated using flow cytometry.

Results: The results demonstrated that CAVO decreased the expression of IL-6 and IL-1β in TNF-α- induced HaCaT cells. CAVO significantly reduced the severity of psoriatic symptoms in IMQ-induced mice. The expression of inflammatory cytokines in the skin, such as IL-1β, IL-6, IL-8, IL-22, IL-23, and IL-17 A were decreased, whereas IL-10 levels were increased. The mRNA expressions of TNF-α, IL-23 A, IL-23 R, IL-22, IL-17 A, and RORγt were down-regulated in skin tissues. CAVO also decreased the levels of NF-κB, STAT3, and JAK2 proteins.

Conclusions: CAVO potentially inhibits ILC3s activation to relieve IMQ-induced psoriasis in mice. These effects might be attributed to inhibiting the activation of NF-κB, STAT3, and JAK2 signaling pathways.

Keywords: Cang-ai volatile oil; ILC3s; Psoriasis; Skin-inflammation.

MeSH terms

  • Animals
  • Cytokines / metabolism
  • Disease Models, Animal
  • Imiquimod
  • Immunity, Innate
  • Interleukin-17* / genetics
  • Interleukin-17* / metabolism
  • Interleukin-23 / metabolism
  • Interleukin-6 / metabolism
  • Lymphocytes / metabolism
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Psoriasis* / chemically induced
  • Psoriasis* / drug therapy
  • Skin
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Imiquimod
  • Interleukin-17
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • Interleukin-6
  • Cytokines
  • Interleukin-23