Combination of Astragalus-Salvia and Ophiopogon-Dendrobium herb pairs alleviates Sjögren's Syndrome via inhibiting the JAK1/STAT3 and PI3K/AKT pathways in NOD/Ltj mice.
10.1016/S1875-5364(25)60892-2
- Author:
Peng SUN
1
;
Lili ZHU
1
;
Yang YU
1
;
Sijing HU
1
;
Mengyi SHAN
1
;
Xuan ZHAO
1
;
Xinchang WANG
2
,
3
;
Qiaoyan ZHANG
3
,
4
;
Luping QIN
5
Author Information
1. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310000, China.
2. Department of Rheumatology, the Second Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou 310000, China. Electronic address: ossani@
3. com.
4. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310000, China. Electronic address: zqy1965@
5. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310000, China. Electronic address: lpqin@zcmu.edu.cn.
- Publication Type:Journal Article
- Keywords:
Astragalus-Salvia herb pair;
CXCL9 and CXCL10;
JAK1/STAT3;
Ophiopogon-Dendrobium herb pair;
PI3K/AKT;
Sjgren’s syndrome
- MeSH:
Animals;
STAT3 Transcription Factor/genetics*;
Sjogren's Syndrome/immunology*;
Mice, Inbred NOD;
Proto-Oncogene Proteins c-akt/genetics*;
Phosphatidylinositol 3-Kinases/genetics*;
Mice;
Drugs, Chinese Herbal/administration & dosage*;
Signal Transduction/drug effects*;
Janus Kinase 1/genetics*;
Humans;
Female;
Astragalus Plant/chemistry*;
Male
- From:
Chinese Journal of Natural Medicines (English Ed.)
2025;23(6):733-741
- CountryChina
- Language:English
-
Abstract:
Sjögren's syndrome (SS) is an autoimmune disease characterized primarily by oral and periocular dryness. Astragalus-Salvia (AS) and Ophiopogon-Dendrobium (OD) represent two frequently utilized herb pairs in SS treatment. While the combination of AS-OD herb pairs demonstrates clinical efficacy in alleviating SS symptoms, its underlying mechanism remains unclear. This investigation sought to assess the therapeutic effects and elucidate the potential mechanisms of AS-OD in non-obese diabetic (NOD)/Ltj mice with SS. The study utilized NOD/Ltj mice as SS models, administering AS-OD treatment for 10 weeks at doses of 113.1, 226.2, and 339.3 mg·d-1·20 g-1. Results demonstrated that AS-OD improved SS symptoms, evidenced by enhanced salivary flow rate, decreased anti-SSA/Ro and anti-SSB/La antibody levels, increased swimming duration, and reduced lactate (LA) and blood urea nitrogen (BUN) levels in NOD/Ltj mice. AS-OD reduced lymphocyte infiltration, enhanced Aquaporin-5 (AQP5) expression in the submandibular gland, decreased inflammatory cytokine levels in the submandibular gland, and reduced the T helper type 17/regulatory T lymphocyte (Th17/Treg) cell ratio in the spleen. Transcriptomic and proteomic analyses indicated AS-OD's involvement in regulating phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and Janus kinase 3/signal transducer and activator of transcription 3 (JAK1/STAT3) pathways, with inhibitory effects validated in both NOD/Ltj mice submandibular gland and A-253 cells. Furthermore, AS-OD enhanced cell viability and reduced A-253 cell apoptosis through the PI3K/AKT pathway. In A-253 cells, AS-OD reduced inflammatory cytokine levels, CXC chemokine ligand 9/10 (CXCL9/10), and T-cell chemotaxis by inhibiting the JAK1/STAT3 pathway. AS-OD mitigates SS by suppressing inflammation and immune responses through the PI3K/AKT and JAK1/STAT3 pathways.
