Journal of ethnopharmacology · 2026
Mechanism exploration of Jiajian Yiguan decoction in treating Sjögren's syndrome.
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Liu Erxiong, Gao Le-Nyu, Wang Yong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Sjögren's syndrome (SS) is a chronic systemic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands and a lack of effective therapeutic options. Jiajian Yiguan Decoction (JYD) has demonstrated promising clinical efficacy in SS patients, yet its underlying mechanism remains unclear.
AIM OF THE STUDY: This study aimed to evaluate the therapeutic effect of JYD in a murine model of SS and to explore its potential mechanism involving the nuclear factor kappa B (NF-κB)-aquaporin 5 (AQP5) signaling pathway.
MATERIALS AND METHODS: The chemical constituents of JYD granules were analyzed using UPLC-ESI-MS/MS. Female ICR mice served as normal controls, while female non-obese diabetic (NOD)/ShiLtJ mice, a well-established SS model, were randomly assigned to five groups: SS, SS + hydroxychloroquine (HCQ), and SS + high-, moderate-, and low-dose JYD. The following parameters were assessed: histopathological changes in submandibular gland tissue (hematoxylin-eosin staining), CD4+/CD8+ T lymphocyte ratios (immunofluorescence), AQP5 expression (immunohistochemistry), serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and anti-AQP5 autoantibodies (enzyme-linked immunosorbent assay); protein expression of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), AQP5, and inhibitory kappa B-alpha (IκB-α) (Western blot); NF-κB DNA-binding activity (electrophoretic mobility shift assay, EMSA); and NF-κB subunit composition (supershift EMSA).
RESULTS: UPLC-ESI-MS/MS identified a total of 95 chemical components in JYD. Compared with the SS group, JYD-treated mice exhibited significantly reduced water intake, diminished lymphocytic infiltration, and less acinar cell destruction in the submandibular glands. Serum concentrations of TNF-α, IL-1β, IL-6, and anti-AQP5 antibodies were also markedly lower. High- and moderate-dose JYD groups showed significantly decreased TLR4 and MyD88 protein expression relative to the SS group. Concurrently, JYD treatment significantly upregulated AQP5 and IκB-α expression and substantially suppressed NF-κB DNA-binding activity.
CONCLUSION: JYD exerts therapeutic effects in SS model mice, likely by inhibiting the NF-κB signaling pathway, enhancing AQP5 protein expression, and thereby attenuating the production of proinflammatory cytokines.
AIM OF THE STUDY: This study aimed to evaluate the therapeutic effect of JYD in a murine model of SS and to explore its potential mechanism involving the nuclear factor kappa B (NF-κB)-aquaporin 5 (AQP5) signaling pathway.
MATERIALS AND METHODS: The chemical constituents of JYD granules were analyzed using UPLC-ESI-MS/MS. Female ICR mice served as normal controls, while female non-obese diabetic (NOD)/ShiLtJ mice, a well-established SS model, were randomly assigned to five groups: SS, SS + hydroxychloroquine (HCQ), and SS + high-, moderate-, and low-dose JYD. The following parameters were assessed: histopathological changes in submandibular gland tissue (hematoxylin-eosin staining), CD4+/CD8+ T lymphocyte ratios (immunofluorescence), AQP5 expression (immunohistochemistry), serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and anti-AQP5 autoantibodies (enzyme-linked immunosorbent assay); protein expression of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), AQP5, and inhibitory kappa B-alpha (IκB-α) (Western blot); NF-κB DNA-binding activity (electrophoretic mobility shift assay, EMSA); and NF-κB subunit composition (supershift EMSA).
RESULTS: UPLC-ESI-MS/MS identified a total of 95 chemical components in JYD. Compared with the SS group, JYD-treated mice exhibited significantly reduced water intake, diminished lymphocytic infiltration, and less acinar cell destruction in the submandibular glands. Serum concentrations of TNF-α, IL-1β, IL-6, and anti-AQP5 antibodies were also markedly lower. High- and moderate-dose JYD groups showed significantly decreased TLR4 and MyD88 protein expression relative to the SS group. Concurrently, JYD treatment significantly upregulated AQP5 and IκB-α expression and substantially suppressed NF-κB DNA-binding activity.
CONCLUSION: JYD exerts therapeutic effects in SS model mice, likely by inhibiting the NF-κB signaling pathway, enhancing AQP5 protein expression, and thereby attenuating the production of proinflammatory cytokines.