Electroacupuncture alleviates acute gouty arthritis by inhibiting NLRP3 inflammasome activation via modulation of the circadian-inflammation axis
- Int Immunopharmacol. 2026 Jun 15:179:116650. doi: 10.1016/j.intimp.2026.116650.
- 1. Department of Nephrology and Rheumatology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China.
- 2. The First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
- 3. Department of Traditional Chinese Internal Medicine, Southern Medical University, Guangzhou, China.
- 4. Guangzhou University of Traditional Chinese Medicine, China.
- 5. The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China.
- 6. Guangzhou Medical University, Guangzhou, China.
- 7. Department of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China. Electronic address: [email protected].
- 8. Guangzhou University of Traditional Chinese Medicine, China. Electronic address: [email protected].
- 9. Department of Nephrology and Rheumatology, The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, China. Electronic address: [email protected].
Electroacupuncture (EA) has shown anti-inflammatory potential in gouty arthritis (GA). This study aimed to investigate its therapeutic effects and underlying mechanisms. Core acupoints (ST36 and SP6) were identified through data-mining. In MSU-induced GA rats, EA significantly alleviated joint swelling, improved gait, reduced serum TNF-α, IL-6 and IL-1β, and suppressed synovial inflammatory infiltration. Mechanistically, EA downregulated NLRP3, Caspase-1 and IL-1β in joint tissue. Further analyses revealed that EA modulates sciatic nerve signaling, influences the central circadian clock in the suprachiasmatic nucleus, and restores rhythmic expression of peripheral circadian genes (e.g., Bmal1, Rev-erbα), thereby inhibiting NLRP3 inflammasome activation. In conclusion, EA at ST36 and SP6 ameliorates acute GA by regulating the circadian-inflammation axis and suppressing NLRP3 inflammasome activation, providing experimental evidence for EA as a promising therapy for gout, although further translational studies are warranted to confirm its clinical applicability.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Autophagy; Microtubule/Tubulin; Environmental Pollutants; NOD-like Receptor (NLR); ApoptosisResearch Areas: Cancer
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target: Cytochrome P450Research Areas: Metabolic Disease