1. Academic Validation
  2. Effect of peiminine on DNCB-induced atopic dermatitis by inhibiting inflammatory cytokine expression in vivo and in vitro

Effect of peiminine on DNCB-induced atopic dermatitis by inhibiting inflammatory cytokine expression in vivo and in vitro

  • Int Immunopharmacol. 2018 Mar:56:135-142. doi: 10.1016/j.intimp.2018.01.025.
Jeong-Min Lim 1 Bina Lee 1 Ju-Hee Min 1 Eun-Young Kim 1 Jae-Hyun Kim 1 SooYeon Hong 1 Jwa-Jin Kim 2 Youngjoo Sohn 3 Hyuk-Sang Jung 4
Affiliations

Affiliations

  • 1 Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea.
  • 2 Department of Medical Science, Brain Research Institute, School of Medicine, Chungnam National University, 266, Munhwa-ro, Jung-gu, Daejeon 35015, Republic of Korea; LES Corporation Inc. R&D Center, 109Ho, 266, Munhwa-ro, Jung-gu, Daejeon 35015, Republic of Korea.
  • 3 Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea. Electronic address: [email protected].
  • 4 Department of Anatomy, College of Korean Medicine, Kyung Hee University, Seoul 02447, Republic of Korea. Electronic address: [email protected].
Abstract

Peiminine (PMN) is the main component derived from Fritillaria ussuriensis and is used in traditional medicine in East Asia. The aim of this study was to evaluate the effects of PMN on atopic dermatitis (AD) induced by a dinitrochlorobenzene (DNCB) in Balb/c mice. Inflammatory cytokine expression of PMN was investigated in vitro. Eosinophil infiltration and the thickness of DNCB-induced AD mouse skin were measured. The levels of IgE, IL-4, IL-6, IL-13, and TNF-α in the serum were measured by ELISA. The effects of PMN on the transcription level of MAPK and nuclear factor (NF)-κB were evaluated in mouse skin. In addition, the inhibitory effect of TNF-α, IL-1β, COX-2 and PGE2 were measured in RAW264.7 cells; TARC was investigated in HaCaT cells; and β-hexosaminidase was examined in RBL-2H3 cells. PMN decreased the number of eosinophils in the dermis as well as mast cells and decreased the thickness of the epidermis and dermis. The PMN High group had a significantly reduced serum level of IgE, IL-4, IL-13 and TNF-α. Moreover, P-ERK and P-P38 were inhibited in the PMN High group compared with the DNCB-treated group. PMN additionally attenuated the expression of inflammatory cytokines in cells, including RAW264.7, HaCaT and RBL-2H3 cells. Our results suggest that PMN could be a potential therapeutic candidate for the treatment of AD.

Keywords

Atopic dermatitis; Eosinophil infiltration; IgE; Inflammatory cytokines; Mast cell; Peiminine.

Figures
Products