Department of Dermatology, Hubei Provincial Hospital of Traditional Chinese Medicine, No. 4 Huayuanshan, Wuchang District, Wuhan, Hubei Province, 430061, China.
Arch Dermatol Res. 2024 Jun 7;316(7):348. doi: 10.1007/s00403-024-03002-3.
This study investigates the mechanism through which paeoniflorin inhibits TSLP expression to regulate dendritic cell activation in corticosteroid-dependent dermatitis treatment. Utilizing databases like TCMSP, we identified paeoniflorin's components, targets, and constructed networks. Molecular docking and gene enrichment analysis helped pinpoint key targets and pathways affected by paeoniflorin. In vitro and in vivo models were used to study CD80, CD86, cytokines, T-cell activation, skin lesions, histopathological changes, TSLP, CD80, and CD86 expression. Our study revealed paeoniflorin's active constituent targeting IL-6 in corticosteroid-dependent dermatitis. In vitro experiments demonstrated reduced TSLP expression, CD80, CD86, and cytokine secretion post-paeoniflorin treatment. In vivo, paeoniflorin significantly decreased skin lesion severity, cytokine levels, TSLP, CD80, and CD86 expression. The study highlights paeoniflorin's efficacy in inhibiting TSLP expression and suppressing dendritic cell activation in corticosteroid-dependent dermatitis, suggesting its potential as a therapeutic intervention. Additionally, it offers insights into the complex molecular mechanisms underlying paeoniflorin's anti-inflammatory properties in treating corticosteroid-dependent dermatitis.
本研究旨在探讨芍药苷通过抑制 TSLP 表达来调节皮质类固醇依赖性皮炎治疗中树突状细胞激活的机制。利用 TCMSP 等数据库，我们鉴定了芍药苷的成分、靶点，并构建了网络。分子对接和基因富集分析有助于确定芍药苷影响的关键靶点和途径。我们使用体外和体内模型研究了 CD80、CD86、细胞因子、T 细胞激活、皮肤损伤、组织病理学变化、TSLP、CD80 和 CD86 的表达。我们的研究揭示了芍药苷在皮质类固醇依赖性皮炎中靶向 IL-6 的活性成分。体外实验表明，芍药苷处理后 TSLP 表达、CD80、CD86 和细胞因子分泌减少。在体内，芍药苷显著降低了皮肤损伤的严重程度、细胞因子水平、TSLP、CD80 和 CD86 的表达。该研究强调了芍药苷抑制 TSLP 表达和抑制皮质类固醇依赖性皮炎中树突状细胞激活的功效，提示其作为治疗干预的潜力。此外，它还深入了解了芍药苷在治疗皮质类固醇依赖性皮炎中的抗炎作用的复杂分子机制。
