ReferenceID 1776
The potential of Diosgenin in treating psoriasis: Studies from HaCaT keratinocytes and imiquimod-induced murine model
Life Sci
AIMS: Psoriasis is a cutaneous disease mainly characterized by keratinocyte hyperproliferation, abnormal epidermal differentiation, inflammation and angiogenesis. In this study, we aimed to report the therapeutic potenti
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- Reference Id
- 1776
- Evidence Id
- 18366
- Core Evidence Id
- 18366
- Source Reference Id
- 3545
- Herb2 Reference Id
- HBREF004342
- Subject Paper Key
- HBIN024164_31790685
- Pubmed Id
- 31790685
- Doi
- 10.1016/j.lfs.2019.117115
- Paper Title
- The potential of Diosgenin in treating psoriasis: Studies from HaCaT keratinocytes and imiquimod-induced murine model
- Paper Abstract
- AIMS: Psoriasis is a cutaneous disease mainly characterized by keratinocyte hyperproliferation, abnormal epidermal differentiation, inflammation and angiogenesis. In this study, we aimed to report the therapeutic potential of Diosgenin on psoriasis-like models and explore the underlying mechanisms. MAIN METHODS: For in vitro studies, we initially evaluated the bioeffects of Diosgenin on keratinocytes by detecting the cell viability, cell cycle and apoptosis in HaCaT cells. To mimic psoriatic conditions, we established hyperproliferative model by stimulating HaCaT cells with LPS/IL-22 and inflammatory model by LPS/TNF-alpha stimulation. Meanwhile, differentiation in HaCaT cells and angiogenesis in HUVECs/HMEC-1 were observed. The influence of Diosgenin on above-mentioned conditions was examined. For in vivo studies, we dosed imiquimod (IMQ) -induced mice with Diosgenin and conducted hematoxylin-eosin (HE), TUNEL assay and immunohistochemistry (IHC) to evaluate histological changes, apoptosis and the status of keratinocyte proliferation, epidermal differentiation, vascularity and cutaneous inflammatory cell infiltration respectively. KEY FINDINGS: Results showed that Diosgenin inhibited HaCaT cell growth through cell cycle arrest and NFkappaB inhibition while induced apoptosis by regulating Caspase3, Bax and Bcl-2 protein expression. After Diosgenin treatment, NFkappaB nuclear translocation and IL-22 receptor dependent pathways were suppressed in LPS/IL-22 induced HaCaT cells respectively. Furthermore, Diosgenin downregulated proinflammatory cytokines through TLR4/Myd88 inhibition and upregulated several differentiation markers' expression in HaCaT cells. Additionally, Diosgenin inhibited vascular formation partially by reducing the VEGF-alpha expression in keratinocytes. In animal studies, Diosgenin attenuated psoriatic lesions on mice accordingly. SIGNIFICANCE: This study suggests that Diosgenin might be a promising candidate for developing anti-psoriatic agents.
- Journal
- Life Sci
- Publish Year
- 2020
- Experiment Subject
- mouse; hacat cell; hacat cells; huvecs; il-22 induced hacat cells
- Experiment Type
- Animal Experiment
- Phenotype Related
- Psoriatic Lesions; Psoriasis; Keratinocyte Hyperproliferation; Cutaneous Disease
- Paper Title Cn
- Paper Title En
- The potential of Diosgenin in treating psoriasis: Studies from HaCaT keratinocytes and imiquimod-induced murine model
- Bilingual Status
- semi_complete