Wu Yixing, Yuan Shaoying, Wang Yan, Zhang Yan, Ye Zhiming, Liu Bing, Yang Huiwen, You Tianhui
College of Nursing, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Affiliated Qingyuan Hospital, Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, 511518, China.
Eur J Pharmacol. 2025 Jul 15;999:177433. doi: 10.1016/j.ejphar.2025.177433. Epub 2025 Mar 13.
This study aims to evaluate the effects of α-Bisabolol in the treatment of psoriasis both in vivo and in vitro, and to elucidate its mechanism of action. We used network pharmacology to explore the potential active components and targets of α-Bisabolol in the treatment of psoriasis. Psoriasis-like models were induced in mice or keratinocytes using imiquimod (IMQ) or tumor necrosis factor-α (TNF-α). The results indicated that α-Bisabolol shares 133 potential genes with psoriasis, and pathway enrichment analysis showed that the PI3K/AKT and nuclear factor κB (NF-κB) signaling pathways are considered key pathways. In vivo experiments showed that α-Bisabolol reduced epidermal thickening, inflammatory cell infiltration, and histological psoriasis-like lesions in IMQ-induced mice (P < 0.05, P < 0.01). α-Bisabolol inhibited the elevation of inflammatory cytokines (including interleukin-6(IL-6), interleukin-1β(IL-1β), interleukin-17A(IL-17A), interleukin-23(IL-23) and tumor necrosis factor-α (TNF-α)) in skin lesions of mice and TNF-α-treated HaCat cells (P < 0.05, P < 0.01). Mechanistically, α-Bisabolol inhibited the phosphorylation of PI3K/AKT (PI3K and AKT) and NF-κB (IκB and p65) signaling pathways activated by IMQ (P < 0.05, P < 0.01). Similar changes were detected in TNF-α-treated HaCaT cells. This suggests that α-Bisabolol may inhibit inflammation in TNF-α-treated keratinocytes and psoriasis mice through the PI3K/AKT and NF-κB pathways, providing a new theoretical basis for clinical application in the treatment of psoriasis.
本研究旨在评估α-红没药醇在体内和体外治疗银屑病的效果，并阐明其作用机制。我们运用网络药理学探究α-红没药醇治疗银屑病的潜在活性成分和靶点。使用咪喹莫特（IMQ）或肿瘤坏死因子-α（TNF-α）在小鼠或角质形成细胞中诱导银屑病样模型。结果表明，α-红没药醇与银屑病共有133个潜在基因，通路富集分析显示PI3K/AKT和核因子κB（NF-κB）信号通路被认为是关键通路。体内实验表明，α-红没药醇可减轻IMQ诱导的小鼠表皮增厚、炎性细胞浸润及组织学银屑病样病变（P<0.05，P<0.01）。α-红没药醇可抑制小鼠皮肤损伤及TNF-α处理的HaCaT细胞中炎性细胞因子（包括白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）、白细胞介素-17A（IL-17A）、白细胞介素-23（IL-23）和肿瘤坏死因子-α（TNF-α））的升高（P<0.05，P<0.01）。机制上，α-红没药醇抑制了IMQ激活的PI3K/AKT（PI3K和AKT）和NF-κB（IκB和p65）信号通路的磷酸化（P<0.05，P<0.01）。在TNF-α处理的HaCaT细胞中也检测到了类似变化。这表明α-红没药醇可能通过PI3K/AKT和NF-κB通路抑制TNF-α处理的角质形成细胞和银屑病小鼠中的炎症，为银屑病治疗的临床应用提供了新的理论依据。
