# Single‐Cell RNA Sequencing Reveals the Therapeutic Effects of Electroacupuncture at BL23 on Hyperuricemia‐Induced Nephritis

**Authors:** Yiyang Hu, Xueyan Song, Haichang Li, Songyun Zhao

PMC · DOI: 10.1155/ijog/2494933 · International Journal of Genomics · 2025-11-21

## TL;DR

Electroacupuncture at BL23 reduces kidney inflammation and uric acid levels in mice with hyperuricemia.

## Contribution

This study demonstrates electroacupuncture's therapeutic potential for hyperuricemia-induced kidney injury through specific molecular pathways.

## Key findings

- EA at BL23 lowered serum uric acid and inflammatory markers in HUA mice.
- EA suppressed NLRP3 inflammasome and IL-6/JAK/STAT3 signaling in kidney tissues.
- EA promoted autophagy, reducing kidney inflammation and dysfunction.

## Abstract

Hyperuricemia (HUA) is a metabolic disorder characterized by elevated serum uric acid (UA) level, which would trigger inflammatory processes contributing to kidney damage. Acupuncture stimulation of BL23, a therapeutic strategy in traditional Chinese medicine (TCM), has been reported to promote diuresis and suppress the immune system and seems to be efficacious in HUA. In this study, we aimed to investigate the effect of electroacupuncture (EA) at BL23 on HUA and HUA‐induced kidney inflammation and dysfunction in mice. Mice received EA once daily after being given intragastric potassium oxonate (500 mg/kg) and adenine (100 mg/kg). EA administration not only decreased the levels of serum UA, creatinine, blood urea nitrogen, urinary UA, and protein, along with increased urinary CREA excretion, but also decreased the inflammatory cytokines productions (IL‐1β, IL‐6, and TNF‐α) in serum. scRNA‐seq of treated kidneys revealed that EA at BL23 suppressed the NLRP3 inflammasome complex, the IL‐6/JAK/STAT3 signaling pathway, and the production of IL‐6 and IL‐1β in HUA mice. Western blot analyses verified that EA suppressed the HUA‐induced NLRP3 inflammasome activation by promoting autophagy. In conclusion, the study demonstrated that EA at BL23 exhibited anti‐HUA and nephroprotective effects by inhibiting both the NLRP3 inflammasome and the IL‐6/JAK/STAT3 signaling pathway, reducing renal inflammation and supporting its therapeutic potential for HUA‐associated kidney injury.

## Linked entities

- **Genes:** NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548], IL1B (interleukin 1 beta) [NCBI Gene 3553], IL6 (interleukin 6) [NCBI Gene 3569], TNF (tumor necrosis factor) [NCBI Gene 7124], jak (Janus kinase) [NCBI Gene 778659], STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774]
- **Chemicals:** uric acid (PubChem CID 1175), creatinine (PubChem CID 588), potassium oxonate (PubChem CID 2723920), adenine (PubChem CID 190)
- **Diseases:** hyperuricemia (MONDO:0002144), nephritis (MONDO:0001166)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Nlrp3 (NLR family, pyrin domain containing 3) [NCBI Gene 216799] {aka AGTAVPRL, AII/AVP, Cias1, FCAS, FCU, MWS}, Stat3 (signal transducer and activator of transcription 3) [NCBI Gene 20848] {aka 1110034C02Rik, Aprf}
- **Diseases:** Nephritis (MESH:D009393), metabolic disorder (MESH:D008659), HUA (MESH:D033461), kidney damage (MESH:D007674), inflammatory (MESH:D007249)
- **Chemicals:** creatinine (MESH:D003404), urea nitrogen (MESH:C530477), BL23 (-), adenine (MESH:D000225), potassium oxonate (MESH:C489337), UA (MESH:D014527)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

11 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12638432/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12638432/full.md

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Source: https://tomesphere.com/paper/PMC12638432