Therapeutic Effects of Methanol Extract from Euphorbia kansui Radix on Imiquimod-Induced Psoriasis.
Soo Jeong KimYe Won JangKyung Eun HyungDa Kyoung LeeKee Hyeob HyunSo-Young ParkEon-Sub ParkKwang Woo HwangPublished in: Journal of immunology research (2017)
The roots of Euphorbia kansui, which belong to the family Euphorbiaceae, have been used as a traditional medicine for the treatment of various diseases such as diabetes, ascites, and leukemia. Recently, it was reported that the methylene chloride fraction of E. kansui radix (EKC) regulated the differentiation of Th17 cells and alleviated the symptoms of Th17-related inflammatory bowel disease. Imiquimod (IMQ), a TLR7/8 agonist, has been used to induce psoriasis in a mouse model. In this study, we evaluated the effect of EKC in an IMQ-induced psoriasis model. EKC effectively inhibited the production of interleukin-17A and interferon-γ in vitro. On this basis, EKC was administered to an animal model of psoriasis. Acanthosis and the infiltration of inflammatory cells into the dermis were significantly reduced by EKC. EKC also inhibited the expression of IL-17A, IL-22, IL-23, IL-12, and RAR-related orphan receptor gamma t (RORγt) in the spleen, skin-draining lymph nodes, and the skin. Additionally, EKC inhibited the activity of dendritic cells but not that of keratinocytes. In conclusion, EKC ameliorated the symptoms of psoriasis through inhibition of Th17 differentiation and activation of dendritic cells. These effects are expected to be beneficial in the treatment and prevention of psoriasis.
Keyphrases
- dendritic cells
- induced apoptosis
- immune response
- mouse model
- lymph node
- atopic dermatitis
- cell cycle arrest
- type diabetes
- oxidative stress
- high glucose
- diabetic rats
- acute myeloid leukemia
- regulatory t cells
- poor prognosis
- cardiovascular disease
- drug induced
- toll like receptor
- bone marrow
- adipose tissue
- endoplasmic reticulum stress
- depressive symptoms
- sleep quality
- inflammatory response
- early stage
- endothelial cells
- signaling pathway
- nuclear factor
- cell proliferation
- metabolic syndrome
- neoadjuvant chemotherapy
- glycemic control