Fitoterapia · 2026
Mechanistic insight into Solanum lyratum Thunb. extract for ameliorating imiquimod-induced psoriasis in mice via suppression of mast cell and Th17 cell response.
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Jin Shuo, Chen Jiahui, He Yuqing, Guo Yao, Zhang Jingting, Zhang Zuxing, Ye Fan, Chen Gongxi
Аннотация
OBJECTIVE: To investigate the underlying mechanism of Solanum lyratum Thunb. (SLT) against psoriasis.
METHODS: A mouse model of psoriasis was established by topical application of imiquimod (IMQ) cream on the nape and dorsal skin. Mice were randomly allocated into the blank control group, model group, SLT treatment groups (low-, medium- and high-dose), and positive control group, with 6 mice in each group. The administration lasted for 7 consecutive days. The skin lesions and pruritic behaviors of mice were observed. Hematoxylin-eosin (H&E) staining was performed to assess the pathological changes of lesional skin and spleen tissues. Toluidine blue staining was used to detect the alterations of mast cells. Immunofluorescence staining was applied to evaluate the changes of T helper 17 (Th17) cells and neutrophils in lesional skin and spleen tissues. Untargeted metabolomics profiling via ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) was conducted to identify differential metabolites in mouse serum, screen potential biomarkers, and analyze the involved metabolic pathways combined with the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Enzyme-linked immunosorbent assay (ELISA) was used to determine the content changes of interleukin (IL)-17A, IL-23, tumor necrosis factor-α (TNF-α), IL-1β, IL-4, interferon-γ (IFN-γ), vascular endothelial growth factor (VEGF), histamine (HIS), and 5-hydroxytryptamine (5-HT) in lesional skin tissues.
RESULTS: SLT alleviated IMQ-induced psoriasis-like skin lesions and spleen edema in mice. SLT ameliorated epidermal hyperplasia and mast cell infiltration in psoriatic lesional skin, and improved inflammatory cell infiltration in both lesional skin and spleen tissues of psoriatic mice. Meanwhile, SLT regulated the levels of Th17 cells and neutrophils in the above two tissues. A total of 30 differential metabolites were screened out via serum metabolomics analysis, which were mainly enriched in signaling pathways including glycerophospholipid metabolism, fatty acid biosynthesis, biosynthesis of unsaturated fatty acids, dysregulated fatty acid metabolism, and Fcγ receptor-mediated phagocytosis. In addition, SLT significantly downregulated the contents of IL-17A, IL-23, IL-1β, HIS and 5-HT in psoriatic lesional skin.
CONCLUSION: SLT exerts a dual anti-psoriatic effect of anti-inflammation and anti-pruritus by inhibiting immune cells such as Th17 cells and mast cells, thereby downregulating inflammatory factors associated with the Th17/IL-23 axis and pruritogens released by activated mast cells. Furthermore, untargeted metabolomics analysis revealed that the anti-psoriatic mechanism of SLT may be closely related to lipid metabolism disorder, a hallmark pathological feature of psoriasis.
METHODS: A mouse model of psoriasis was established by topical application of imiquimod (IMQ) cream on the nape and dorsal skin. Mice were randomly allocated into the blank control group, model group, SLT treatment groups (low-, medium- and high-dose), and positive control group, with 6 mice in each group. The administration lasted for 7 consecutive days. The skin lesions and pruritic behaviors of mice were observed. Hematoxylin-eosin (H&E) staining was performed to assess the pathological changes of lesional skin and spleen tissues. Toluidine blue staining was used to detect the alterations of mast cells. Immunofluorescence staining was applied to evaluate the changes of T helper 17 (Th17) cells and neutrophils in lesional skin and spleen tissues. Untargeted metabolomics profiling via ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) was conducted to identify differential metabolites in mouse serum, screen potential biomarkers, and analyze the involved metabolic pathways combined with the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Enzyme-linked immunosorbent assay (ELISA) was used to determine the content changes of interleukin (IL)-17A, IL-23, tumor necrosis factor-α (TNF-α), IL-1β, IL-4, interferon-γ (IFN-γ), vascular endothelial growth factor (VEGF), histamine (HIS), and 5-hydroxytryptamine (5-HT) in lesional skin tissues.
RESULTS: SLT alleviated IMQ-induced psoriasis-like skin lesions and spleen edema in mice. SLT ameliorated epidermal hyperplasia and mast cell infiltration in psoriatic lesional skin, and improved inflammatory cell infiltration in both lesional skin and spleen tissues of psoriatic mice. Meanwhile, SLT regulated the levels of Th17 cells and neutrophils in the above two tissues. A total of 30 differential metabolites were screened out via serum metabolomics analysis, which were mainly enriched in signaling pathways including glycerophospholipid metabolism, fatty acid biosynthesis, biosynthesis of unsaturated fatty acids, dysregulated fatty acid metabolism, and Fcγ receptor-mediated phagocytosis. In addition, SLT significantly downregulated the contents of IL-17A, IL-23, IL-1β, HIS and 5-HT in psoriatic lesional skin.
CONCLUSION: SLT exerts a dual anti-psoriatic effect of anti-inflammation and anti-pruritus by inhibiting immune cells such as Th17 cells and mast cells, thereby downregulating inflammatory factors associated with the Th17/IL-23 axis and pruritogens released by activated mast cells. Furthermore, untargeted metabolomics analysis revealed that the anti-psoriatic mechanism of SLT may be closely related to lipid metabolism disorder, a hallmark pathological feature of psoriasis.