title: A PPARδ-selective antagonist ameliorates IMQ-induced psoriasis-like inflammation in mice.
abstract: PPARδ is highly expressed in skin, especially keratinocytes, and its expression is increased in psoriatic lesions. However, the potential role of PPARδ in the pathogenesis of psoriasis remains undefined. Mice treated with Imiquimod (IMQ) to induce psoriasis can be used to evaluate the pathogenesis of psoriasis, and this model has become one of the most important in vivo research tools for research on the disease. In the current study, we showed that PPARδ was highly expressed in the skin of IMQ-induced psoriasis mice. To further understand the impact of PPARδ in psoriasis, we used these mice in a series of experiments to evaluate the pathogenesis of psoriasis. We found that PPARδ was highly expressed in both psoriatic lesions and normal skin in IMQ-induced psoriasis mice. Furthermore, the expression of PPARδ-relevant lipases was also significantly increased. The PPARδ-selective antagonist GSK3787 ameliorated the observed inflammation in the skin of the experimental mice. Based on these results, PPARδ may be a potential target for the effective treatment of psoriasis.
authors: Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai, China.
authors: Xuguo
authors: X
authors: Wang
authors: Department of Dermatology, 98th Hospital of People's Liberation Army, Anhui Medical University, Huzhou, Zhejiang, China.
authors: Yangyang
authors: Y
authors: Hao
authors: Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Fudan University, China; Shanghai Public Health Clinical Center, Fudan University, China.
authors: Xiaohuan
authors: X
authors: Wang
authors: Changhai Hospital, The Second Military Medical University, Shanghai, China.
authors: Lumei
authors: L
authors: Wang
authors: Department of Health Toxicology, Department of Basic Courses, The Second Military Medical University, Shanghai, China.
authors: Yongchun
authors: Y
authors: Chen
authors: Department of Pharmacy, General Hospital of Jinan Military Area, Jinan, Shandong Province, China.
authors: Jun
authors: J
authors: Sun
authors: Department of Pharmacy, Changhai Hospital, The Second Military Medical University, Shanghai, China. Electronic address: wxh201309@126.com.
authors: Jinhong
authors: J
authors: Hu
mesh_terms: D000634:Aminoquinolines; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001549:Benzamides / Q000494:pharmacology / Q000627:therapeutic use*; D016207:Cytokines / Q000235:genetics; D000077271:Imiquimod; D051379:Mice; D047494:PPAR delta / Q000037:antagonists & inhibitors* / Q000378:metabolism; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000187:drug effects / Q000378:metabolism; D013450:Sulfones / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: C547957:4-chloro-N-(2-((5-trifluoromethyl-2-pyridyl)sulfonyl)ethyl)benzamide; D000634:Aminoquinolines; D000893:Anti-Inflammatory Agents; D001549:Benzamides; D016207:Cytokines; D047494:PPAR delta; D012333:RNA, Messenger; D013450:Sulfones; D000077271:Imiquimod
keywords: PPARδ; Pathogenesis; Psoriasis; Selective antagonist