Research progress on the mechanism of Chinese medicine and active components against cartilage destruction of rheumatoid arthritis
- VernacularTitle:中药及其活性成分改善RA软骨破坏的作用机制研究进展
- Author:
Zhihao DUAN
1
,
2
,
3
,
4
;
You ZHOU
1
,
2
,
3
;
Shigang LI
4
;
Can JIN
4
;
Ying DENG
4
;
Jinlang LIU
1
,
2
,
3
;
Shuai MA
1
,
2
Author Information
1. Dept. of Orthopedics，the Affiliated Renhe Hospital of China Three Gorges University，Hubei Yichang 443001，China
2. Sports Medicine Research Institute，China Three Gorges University，Hubei Yichang 443001，China
3. Clinical Medical Research Center，Yichang Sports Injury and Repair，Hubei Yichang 443001，China
4. Third-grade Pharmacological Laboratory for Traditional Chinese Medicine Approved by State Administration of Traditional Chinese Medicine，China Three Gorges University，Hubei Yichang 443001，China
- Publication Type:Journal Article
- Keywords:
rheumatoid arthritis;
cartilage destruction;
Chinese medicine;
active component;
improvement
- From:
China Pharmacy
2023;34(7):892-896
- CountryChina
- Language:Chinese
-
Abstract:
Rheumatoid arthritis （RA） is a systemic chronic auto-inflammatory disease， characterized by infiltration of inflammatory cells， pannus formation， articular cartilage destruction， and bone matrix destruction. Therefore， improving articular cartilage destruction has an important impact on the treatment of RA. Chinese medicine has a good application effect in improving cartilage destruction of RA due to its characteristics of multiple components， multiple targets， high activity and low side effects. Based on this， the author reviewed relevant literature to summarize the relevant research and mechanism of Chinese medicine and its active components in improving RA cartilage destruction. The results showed that Chinese medicine and its active components can improve RA cartilage destruction by regulating inflammatory factors， phosphatidylinositol 3-kinase/protein kinase B， Wnt/β- catenin， nuclear factor-κB， mitogen-activated protein kinase， Janus kinase 2/signal transduction and activator of transcription 3/ vascular endothelial growth factor， microRNAs， fibroblastic synovial cells.
