Research progress on the mechanisms of traditional Chinese medicine regulating NLRP3 inflammasome to intervene in renal fibrosis
- VernacularTitle:中药调控NLRP3炎症小体干预肾纤维化的作用机制研究进展
- Author:
Chenjie HUANG
1
;
Wenqi YUAN
1
;
Yaohong LU
1
;
Ziyou YAN
1
Author Information
1. Clinical Medical College，Jiangxi University of Chinese Medicine，Nanchang 330004，China
- Publication Type:Journal Article
- Keywords:
NLRP3 inflammasome;
renal fibrosis;
traditional Chinese medicine;
mechanism;
chronic kidney disease
- From:
China Pharmacy
2025;36(18):2334-2340
- CountryChina
- Language:Chinese
-
Abstract:
Renal fibrosis （RF）， characterized by glomerulosclerosis and tubulointerstitial fibrosis， is a central pathological process in chronic kidney disease （CKD）. The nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 （NLRP3） inflammasome is closely linked to the occurrence and progression of RF. This review systematically elucidates the mechanisms of the NLRP3 inflammasome in RF， and summarizes the current research on the inhibition of NLRP3 inflammasome activation by single Chinese herbs， active components of traditional Chinese medicine， Chinese herbal compounds， and Chinese patent medicines for the prevention and treatment of RF. The existing studies have demonstrated that single Chinese herbs （Campanumoea lancifolia， Dioscorea zingiberensis）， active components of traditional Chinese medicine （morroniside， liquiritigenin， rosmarinic acid， magnoflorine， fucoidan， etc.）， Chinese herbal compounds （Bushen huoxue formula， Tongluo yishen decoction， Shizhi formula， Bixie fenqing drink）， and Chinese patent medicine （Suyin jiedu granule） can inhibit the activation of the NLRP3 inflammasome to counteract inflammatory damage. This affects multiple pathways（NLRP3/caspase-1/ gasdermin D， NLRP3/interleukin-1β/Smad， etc.） and related upstream and downstream targets of its activation， effectively reducing pyroptosis， mitigating oxidative stress， promoting mitochondrial autophagy， inhibiting fibroblast activation， and reducing excessive extracellular matrix deposition， thereby exerting anti-RF effects.
