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This study was designed to investigate the inhibitory effects of Angelica polysaccharide (AP) on activation of mast cells and its possible molecular mechanism. In our study, we determined the proinflammatory cytokines and allergic mediators in anti-DNP IgE stimulated RBL-2H3 cells and found that AP (50, 100, and 200 μg/mL) significantly decreased the release of histamine, β-hexosaminidase, leukotrienes C4 (LTC4), IL-1, IL-4, TNF-α, IL-6, and human monocyte chemotactic protein-1 (MCP-1/CCL2) (p < 0.05). In addition, Ca2+ entry was inhibited by treatment with AP. AP also downregulated the protein expressions of p-Fyn, p-Akt, p-P38, IL-4, TNF-α, and NF-κB p65 in both Fyn gene upregulated and normal RBL-2H3 cells (p < 0.05). Collectively, our results showed that AP could inhibit the activation of mast cells via suppressing the releases of proinflammatory cytokines allergic mediators, Gab2/PI3-K/Akt and Fyn/Syk pathways.

As a common chronic skin disease, psoriasis is characterized by the involvement of congenital acquired inflammatory immune diseases. In the study, our results indicated the effect of ginsenoside Rg1 on psoriasis‐like skin and the potential protection mechanisms that have not yet been investigated. In vivo, psoriasis‐like skin mice model was induced by imiquimod (IMQ), then was treated by ginsenoside Rg1 for consecutive 4 weeks to evaluate its effect, respectively. In vitro, M5 cocktail treatment of human immortalized keratinocyte HaCaT‐induced psoriasis‐like skin cell model, which was exposed to ginsenoside Rg1. The inflammatory cell infiltration, expression level of keratinocyte proliferation marker Ki67, keratinocyte proliferation, inflammatory cytokines, and ROS/NLRP3 pathway‐related proteins in vivo and in vitro were examined by hematoxylin and eosin, immunohistochemistry, ELISA, CCK‐8, flow cytometry, and western blot. All results demonstrated that ginsenoside Rg1 attenuated the injury of psoriasis‐like skin, which inhibited the proliferation of skin keratinocytes and the activation of NLRP3 inflammasome and the level of inflammatory factors such as IL‐1β and IL‐18, and decreased the level of Ki67, NLRP3, and caspase‐1 in mice and HaCaT. Furthermore, NLRP3 overexpression attenuates the effect of ginsenoside Rg1 on M5 cocktail‐induced proliferation and NLRP3 inflammasomes in HaCaT. These results demonstrated that ginsenoside Rg1 could suppress the ROS/NLRP3 pathway to treat psoriasis‐like skin. Practical applications This is the very first study to explore the efficacy of ginsenoside Rg1 against psoriasis‐like skin lesions to reveal the underlying mechanism. In this paper, the detection of skin histopathological analysis, CCK‐8, flow cytometry, western blot, and ELISA analysis shows that ginsenoside Rg1 has preventive effect on psoriasis caused by imiquimod or M5 cocktail through inhibiting NLRP3 inflammasome, which helps in the development of novel nutraceutical/functional food against psoriasis and thus could improve the quality of life in psoriasis patients.

The (13)C-MBT is a sensitive tool for the timely detection of acute liver injury and early prediction of recovery in a rat model. Further clinical studies are warranted to validate its role in patients with acute liver injury.

Purpose. Psoriasis is closely linked to ferroptosis. This study aimed to identify potential ferroptosis-associated genes in psoriasis using bioinformatics. Methods. Data from the GSE30999 dataset was downloaded from the Gene Expression Omnibus (GEO), and the ferroptosis-associated genes were retrieved from FerrDb. The differentially expressed ferroptosis-associated genes were identified using Venn diagrams. Subsequently, a network of protein-protein interactions (PPIs) between psoriasis targets and ferroptosis-associated genes was constructed based on the STRING database and analyzed by Cytoscape software. The Metascape portal conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Moreover, the expression of ferroptosis-related genes was verified in the GSE13355 dataset. Finally, the verified genes were used to predict the therapeutic drugs for psoriasis using the DGIdb/CMap database. SwissDock was used to examine ligand docking, and UCSF Chimera displayed the results visually. Results. Among 85 pairs of psoriasis lesion (LS) and no-lesion (NL) samples from patients, 19 ferroptosis-associated genes were found to be differentially expressed (3 upregulated genes and 16 downregulated genes). Based on the PPI results, these ferroptosis-associated genes interact with each other. The GO and KEGG enrichment analysis of differentially expressed ferroptosis-related genes indicated several enriched terms related to the oxidative stress response. The GSE13355 dataset verified the results of the bioinformatics analysis obtained from the GSE30999 dataset regarding SLC7A5, SLC7A11, and CHAC1. Psoriasis-related compounds corresponding to SLC7A5 and SLC7A11 were also identified, including Melphalan, Quisqualate, Riluzole, and Sulfasalazine. Conclusion. We identified 3 differentially expressed ferroptosis-related genes through bioinformatics analysis. SLC7A5, SLC7A11, and CHAC1 may affect the development of psoriasis by regulating ferroptosis. These results open new avenues in understanding the treatment of psoriasis.

Atopic eczema (AE) is a chronic inflammatory skin disease that is mainly characterized by pruritus and epidermal barrier dysfunction. Between 15% and 20% of children and 1%-3% of adults are affected worldwide. AE is a complex disease triggered by multiple triggers, including gene and environmental factors. Impaired skin barrier function, modifications of the immune system, and hyper-reactivity to environmental stimulation directly cause and aggravate AE. In this review, we provide an overview of the recent developments and future directions in the pathogenesis of AE.

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