Frontiers in pharmacology · 2026
Panax notoginseng extract alleviates atopic dermatitis-like skin inflammation associated with suppression of the cGAS-STING pathway.
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Zhu Xu, Wang Yichun, Chen Zhongyi, Zhao Ziyan, Yang Chunhao, Xu Peng, Qu Liping, Wang Feifei, Xiao Fengkun
Аннотация
BACKGROUND: Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by pruritus and xerosis. Current treatments for AD primarily involve glucocorticoids and immunosuppressive agents. However, long-term administration of these treatments may lead to significant adverse effects. Therefore, there is an urgent need for effective therapeutic alternatives with improved safety profiles. Panax notoginseng (Burkill) F. H. Chen is renowned for its diverse pharmacological properties and shows promise in the treatment of skin diseases.
PURPOSE: This study investigated the effects of P. notoginseng extract (PNE) on AD and its underlying mechanisms.
METHODS: We analyzed the chemical composition of PNE using high-performance liquid chromatography (HPLC). The anti-AD effects of PNE were evaluated in both an AD-like mouse model induced by calcipotriol (MC903) and a human keratinocyte (HaCaT) cell model stimulated with tumor necrosis factor-alpha and interferon-gamma (TNF-α/IFN-γ). Furthermore, metabolomics analysis of mouse skin tissue was conducted to elucidate the underlying metabolic mechanisms. To investigate the associated signaling pathways, quantitative real-time PCR (qPCR) and Western blotting were performed.
RESULTS: In MC903-induced mice, PNE exhibited potent anti-AD effects, including attenuation of AD-like skin lesions and suppression of Th2 cytokines (Il-4, Il-13, Il-31) and chemokines (Ccl5, Ccl17, Ccl22). In TNF-α/IFN-γ-stimulated HaCaT cells, PNE dose-dependently inhibited the expression of Th2-associated chemokines (CCL5, CCL17, CCL22). Moreover, PNE suppressed the mRNA expression of cGAS, STING, IRF3, IRF7, and TBK1, as well as the protein levels of cGAS and STING, both in vitro and in vivo. Metabolic profiling of mouse skin tissues revealed that PNE significantly modulates the metabolism of phosphatidylcholine, phosphatidylethanolamine, and arachidonic acid. HPLC analysis showed that ginsenoside Rg1, notoginsenoside R2(S), ginsenoside Rb1, and ginsenoside Rd were the main components of PNE. Notoginsenoside R2(S) and ginsenoside Rd dose-dependently inhibited the mRNA expression of CCL5, CCL17, CCL22, cGAS, STING, IRF3, IRF7, and TBK1.
CONCLUSION: PNE exerts anti-AD effects by attenuating Th2-mediated inflammatory responses via modulation of the cGAS-STING pathway. These findings suggest that PNE has the potential to serve as a natural therapeutic option for AD.
PURPOSE: This study investigated the effects of P. notoginseng extract (PNE) on AD and its underlying mechanisms.
METHODS: We analyzed the chemical composition of PNE using high-performance liquid chromatography (HPLC). The anti-AD effects of PNE were evaluated in both an AD-like mouse model induced by calcipotriol (MC903) and a human keratinocyte (HaCaT) cell model stimulated with tumor necrosis factor-alpha and interferon-gamma (TNF-α/IFN-γ). Furthermore, metabolomics analysis of mouse skin tissue was conducted to elucidate the underlying metabolic mechanisms. To investigate the associated signaling pathways, quantitative real-time PCR (qPCR) and Western blotting were performed.
RESULTS: In MC903-induced mice, PNE exhibited potent anti-AD effects, including attenuation of AD-like skin lesions and suppression of Th2 cytokines (Il-4, Il-13, Il-31) and chemokines (Ccl5, Ccl17, Ccl22). In TNF-α/IFN-γ-stimulated HaCaT cells, PNE dose-dependently inhibited the expression of Th2-associated chemokines (CCL5, CCL17, CCL22). Moreover, PNE suppressed the mRNA expression of cGAS, STING, IRF3, IRF7, and TBK1, as well as the protein levels of cGAS and STING, both in vitro and in vivo. Metabolic profiling of mouse skin tissues revealed that PNE significantly modulates the metabolism of phosphatidylcholine, phosphatidylethanolamine, and arachidonic acid. HPLC analysis showed that ginsenoside Rg1, notoginsenoside R2(S), ginsenoside Rb1, and ginsenoside Rd were the main components of PNE. Notoginsenoside R2(S) and ginsenoside Rd dose-dependently inhibited the mRNA expression of CCL5, CCL17, CCL22, cGAS, STING, IRF3, IRF7, and TBK1.
CONCLUSION: PNE exerts anti-AD effects by attenuating Th2-mediated inflammatory responses via modulation of the cGAS-STING pathway. These findings suggest that PNE has the potential to serve as a natural therapeutic option for AD.