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已发表论文
柴芍润津方改善干燥综合征的药理机制：基于IL-17信号介导炎症级联反应的抑制作用
Authors Gan Y , Du L, Sun Y, Li F, Chen H, Yan S, Xiao X, Li S, Wu B
Received 5 June 2025
Accepted for publication 2 December 2025
Published 10 December 2025 Volume 2025:18 Pages 17289—17308
DOI https://doi.org/10.2147/JIR.S544874
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Shouya Feng
Yu Gan,1,2 Lijing Du,2,3 Yuanfang Sun,2,3 Fugen Li,2 Haoran Chen,2 Shikai Yan,3 Xue Xiao,4 Shasha Li,2,* Bin Wu1,*
1Department of Rheumatology, Chongqing Traditional Chinese Medicine Hospital, Chongqing, People’s Republic of China; 2The Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, People’s Republic of China; 3School of Pharmacy, Shanghai Jiao Tong University, Shanghai, People’s Republic of China; 4Institute of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Bin Wu; Shasha Li, Email wuubinn@126.com; happylishasha@163.com
Background: Sjögren’s Syndrome (SS) is the second most prevalent autoimmune disease in China without effective therapy. Current evidence indicates safety and effectiveness of CheReCunJin formula (CRCJ) in treating SS. However, the underlying mechanism remains unclear.
Methods: UPLC-Q-TOF-MS was applied for compound identification. Multiple components, targets and pathways involved in the treatment of SS with CRCJ were predicted by network pharmacology. Molecular docking was used for preliminary validation. NOD mouse, a classic spontaneous SS model, was used to examine the therapeutic effects on SS of CRCJ. The potential mechanism of CRCJ to mitigate SS was investigated by serum untargeted metabolomics. Validation of key pathway and targets was conducted using flow cytometry, ELISA, immunohistochemistry, Masson staining, and Western blot.
Results: 373 compounds were identified in CRCJ. Through network pharmacology and molecular docking, 15 main components (eg, luteolin 7-O-β-D-glucoside, rutin, 1,4-dicaffeoylquinic acid, anemarsaponin C), 10 core targets (including HSP90AA1, TNF, MMP9, MAPK1, IL6), and the key pathway for CRCJ treating SS, IL-17 signaling pathway, were screened out. In NOD mice, CRCJ demonstrated the ability to improve salivary flow rate and water intake, reduce submandibular gland (SMG) tissue damage, and diminished the levels of IFN-α, IFN-β, IgG in serum. CRCJ modulated metabolic disorders, differentially regulating 63 metabolites and 6 metabolic pathways. Additional validation showed that CRCJ inhibited the Th17 cell activation, downregulated IL-17 signal transduction, and improved ECM degradation in SMG.
Conclusion: CRCJ protected salivary glands in SS by inhibiting IL-17 signal-mediated inflammatory cascade, an effect likely attributable to key bioactive components such as luteolin 7-O-β-D-glucoside, rutin, 1,4-dicaffeoylquinic acid, and anemarrhenasaponin C. This study provides a foundation for the further development and clinical application of CRCJ for the treatment of SS.
Keywords: CheReCunJin formula, IL-17 signal pathway, inflammatory cascade, metabolomics, network pharmacology, Sjögren’s syndrome
1Department of Rheumatology, Chongqing Traditional Chinese Medicine Hospital, Chongqing, People’s Republic of China; 2The Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, People’s Republic of China; 3School of Pharmacy, Shanghai Jiao Tong University, Shanghai, People’s Republic of China; 4Institute of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Bin Wu; Shasha Li, Email wuubinn@126.com; happylishasha@163.com
Background: Sjögren’s Syndrome (SS) is the second most prevalent autoimmune disease in China without effective therapy. Current evidence indicates safety and effectiveness of CheReCunJin formula (CRCJ) in treating SS. However, the underlying mechanism remains unclear.
Methods: UPLC-Q-TOF-MS was applied for compound identification. Multiple components, targets and pathways involved in the treatment of SS with CRCJ were predicted by network pharmacology. Molecular docking was used for preliminary validation. NOD mouse, a classic spontaneous SS model, was used to examine the therapeutic effects on SS of CRCJ. The potential mechanism of CRCJ to mitigate SS was investigated by serum untargeted metabolomics. Validation of key pathway and targets was conducted using flow cytometry, ELISA, immunohistochemistry, Masson staining, and Western blot.
Results: 373 compounds were identified in CRCJ. Through network pharmacology and molecular docking, 15 main components (eg, luteolin 7-O-β-D-glucoside, rutin, 1,4-dicaffeoylquinic acid, anemarsaponin C), 10 core targets (including HSP90AA1, TNF, MMP9, MAPK1, IL6), and the key pathway for CRCJ treating SS, IL-17 signaling pathway, were screened out. In NOD mice, CRCJ demonstrated the ability to improve salivary flow rate and water intake, reduce submandibular gland (SMG) tissue damage, and diminished the levels of IFN-α, IFN-β, IgG in serum. CRCJ modulated metabolic disorders, differentially regulating 63 metabolites and 6 metabolic pathways. Additional validation showed that CRCJ inhibited the Th17 cell activation, downregulated IL-17 signal transduction, and improved ECM degradation in SMG.
Conclusion: CRCJ protected salivary glands in SS by inhibiting IL-17 signal-mediated inflammatory cascade, an effect likely attributable to key bioactive components such as luteolin 7-O-β-D-glucoside, rutin, 1,4-dicaffeoylquinic acid, and anemarrhenasaponin C. This study provides a foundation for the further development and clinical application of CRCJ for the treatment of SS.
Keywords: CheReCunJin formula, IL-17 signal pathway, inflammatory cascade, metabolomics, network pharmacology, Sjögren’s syndrome