Drug design, development and therapy · 2026
Sophocarpine Alleviates Airway Epithelial Cell Inflammation in Asthma via Modulating the Cytokine- Cytokine Receptor and JAK2/STAT3 Signaling Pathways.
СтатьяНазвание и аннотация: Перевод в очереди
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Zhi Wenbing, Zhang Hong, Qiao Ziyao, Jiang Shengnan, Liang Zongsuo, Liu Yang
Аннотация
PURPOSE: Asthma is a complex, heterogeneous, and inflammatory disease with an increasing incidence worldwide. This study aimed to investigate the therapeutic mechanisms of sophocarpine in asthma systematically.
METHODS: A house dust mite (HDM)-induced mouse and cell model was built. The effects and mechanisms of sophocarpine on asthma were evaluated in vivo and in vitro.
RESULTS: In the mouse model, sophocarpine treatment reduced airway pathological damage, mucus secretion, levels of interleukin (IL)-4, IL-5, IL-17, immunoglobulin E (IgE), and splenic index, as well as eosinophil accumulation. Network pharmacology studies revealed that sophocarpine may target TLR4, STAT3, and TNF, and regulates the JAK-STAT, and Viral protein interaction with cytokine and cytokine receptor signaling pathway et al. Docking results showed that the binding energy of sophocarpine to major targets varied from -7.55 to -5.22 kcal/mol. Transcriptome analysis identified 436 DEGs, which were enriched in pathways consistent with the network pharmacology, such as the JAK-STAT signaling pathway. We further confirmed that sophocarpine downregulated the mRNA expression levels of CCL5, CCL7, CCL12, CXCL1, CXCL2, CXCL3, CCR2, CXCR2, CXCR3, JAK2, STAT3, and c-MYC, and protein expression of CXCR2, JAK2, STAT3, and c-MYC in the mouse model. Sophocarpine also inhibited HDM-induced BEAS-2B cell viability decrease, cell apoptosis, and ROS overproduction, which was associated with modulation of the cytokine-cytokine receptor and JAK-STAT signaling pathways. Further, similar to sophocarpine, STAT3 inhibitors and siRNA effectively reduced the levels of STAT3, MYC, and CXCR2.
CONCLUSION: These results indicate that sophocarpine effectively inhibits HDM-induced airway epithelial cell inflammation through regulating cytokine-cytokine receptor and JAK2/STAT3 signaling pathways.
METHODS: A house dust mite (HDM)-induced mouse and cell model was built. The effects and mechanisms of sophocarpine on asthma were evaluated in vivo and in vitro.
RESULTS: In the mouse model, sophocarpine treatment reduced airway pathological damage, mucus secretion, levels of interleukin (IL)-4, IL-5, IL-17, immunoglobulin E (IgE), and splenic index, as well as eosinophil accumulation. Network pharmacology studies revealed that sophocarpine may target TLR4, STAT3, and TNF, and regulates the JAK-STAT, and Viral protein interaction with cytokine and cytokine receptor signaling pathway et al. Docking results showed that the binding energy of sophocarpine to major targets varied from -7.55 to -5.22 kcal/mol. Transcriptome analysis identified 436 DEGs, which were enriched in pathways consistent with the network pharmacology, such as the JAK-STAT signaling pathway. We further confirmed that sophocarpine downregulated the mRNA expression levels of CCL5, CCL7, CCL12, CXCL1, CXCL2, CXCL3, CCR2, CXCR2, CXCR3, JAK2, STAT3, and c-MYC, and protein expression of CXCR2, JAK2, STAT3, and c-MYC in the mouse model. Sophocarpine also inhibited HDM-induced BEAS-2B cell viability decrease, cell apoptosis, and ROS overproduction, which was associated with modulation of the cytokine-cytokine receptor and JAK-STAT signaling pathways. Further, similar to sophocarpine, STAT3 inhibitors and siRNA effectively reduced the levels of STAT3, MYC, and CXCR2.
CONCLUSION: These results indicate that sophocarpine effectively inhibits HDM-induced airway epithelial cell inflammation through regulating cytokine-cytokine receptor and JAK2/STAT3 signaling pathways.