Huayu Fan1, Yao Wang2, Xilin Zhang3, Jinguang Chen4, Qianqian Zhou2, Zengyang Yu2, Youdong Chen2, Zeyu Chen2, Jun Gu5, Yuling Shi6. 1. Department of Dermatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China; Institute of Psoriasis, Tongji University School of Medicine, Shanghai, 200072, China; Department of Dermatology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, 318000, China. 2. Department of Dermatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China; Institute of Psoriasis, Tongji University School of Medicine, Shanghai, 200072, China. 3. Institute of Psoriasis, Tongji University School of Medicine, Shanghai, 200072, China; Department of Dermatology, Shanghai Skin Disease Hospital, Shanghai, 200443, China. 4. Department of Dermatology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, 318000, China. 5. Institute of Psoriasis, Tongji University School of Medicine, Shanghai, 200072, China; Department of Dermatology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, 200443, China. Electronic address: gujun79@163.com. 6. Department of Dermatology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China; Institute of Psoriasis, Tongji University School of Medicine, Shanghai, 200072, China. Electronic address: shiyuling1973@tongji.edu.cn.
Abstract
BACKGROUND: Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation. Ginsenoside compound K (CK), a bioactive metabolite of ginseng, modulates various skin disorders with an impact on keratinocyte biology. However, the effect of Ginsenoside CK in psoriasis has not been explored. OBJECTIVE: Our aim was to investigate whether ginsenoside CK could affect the homeostasis of keratinocytes and their expression of psoriasis-associated antimicrobial protein regenerating islet-derived protein 3-alpha (REG3A) and its murine ortholog RegIIIγ. We further explored the therapeutic potential of ginsenoside CK in imiquimod (IMQ)-induced psoriasis-like dermatitis. METHODS: The effects of ginsenoside CK in cell growth and apoptosis of human keratinocytes were measured by MTT assay and flow cytometry, respectively. Bax levels were evaluated by Western blot in HaCaT cells following ginsenoside CK stimulation. REG3A levels were assessed by RT-PCR and Western blot in human keratinocytes following interleukin (IL)-36γ and ginsenoside CK co-simulation. Utilizing IMQ-induced psoriasis mouse model, the therapeutic effects of 0.1% and 1% ginsenoside CK cream were assessed by skin thicknesses and histological examinations, and RegIIIγ level in the lesional skin was detected by Western blot and immunofluorescence. RESULTS: Ginsenoside CK prohibited human keratinocyte proliferation but did not affect their apoptosis. Moreover, it inhibited IL-36γ-induced REG3A expression in HaCaT cells. Ginsenoside CK alleviated imiquimod-induced psoriasis-like hyperkeratosis and reduced RegIIIγ expression in the keratinocytes from lesional skin. CONCLUSION: Ginsenoside CK ameliorated IMQ-induced psoriasis-like dermatitis possibly through inhibiting REG3A/RegIIIγ expression in keratinocytes, which highlighted a therapeutic potential of ginsenoside CK in psoriasis.
BACKGROUND:Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation. Ginsenoside compound K (CK), a bioactive metabolite of ginseng, modulates various skin disorders with an impact on keratinocyte biology. However, the effect of Ginsenoside CK in psoriasis has not been explored. OBJECTIVE: Our aim was to investigate whether ginsenoside CK could affect the homeostasis of keratinocytes and their expression of psoriasis-associated antimicrobial protein regenerating islet-derived protein 3-alpha (REG3A) and its murine ortholog RegIIIγ. We further explored the therapeutic potential of ginsenoside CK in imiquimod (IMQ)-induced psoriasis-like dermatitis. METHODS: The effects of ginsenoside CK in cell growth and apoptosis of human keratinocytes were measured by MTT assay and flow cytometry, respectively. Bax levels were evaluated by Western blot in HaCaT cells following ginsenoside CK stimulation. REG3A levels were assessed by RT-PCR and Western blot in human keratinocytes following interleukin (IL)-36γ and ginsenoside CK co-simulation. Utilizing IMQ-induced psoriasismouse model, the therapeutic effects of 0.1% and 1% ginsenoside CK cream were assessed by skin thicknesses and histological examinations, and RegIIIγ level in the lesional skin was detected by Western blot and immunofluorescence. RESULTS:Ginsenoside CK prohibited human keratinocyte proliferation but did not affect their apoptosis. Moreover, it inhibited IL-36γ-induced REG3A expression in HaCaT cells. Ginsenoside CK alleviated imiquimod-induced psoriasis-like hyperkeratosis and reduced RegIIIγ expression in the keratinocytes from lesional skin. CONCLUSION:Ginsenoside CK ameliorated IMQ-induced psoriasis-like dermatitis possibly through inhibiting REG3A/RegIIIγ expression in keratinocytes, which highlighted a therapeutic potential of ginsenoside CK in psoriasis.