NETWORK PHARMACOLOGY ANALYSIS OF THE ANTI- INFLAMMATORY MECHANISMS OF WENQING BITONG DECOCTION IN RHEUMATOID ARTHRITIS

Tóm tắt

Background: Rheumatoid arthritis is a chronic autoimmune disease involving complex inflammatory networks and multiple pathogenic pathways. Although Wenqing Bitong Decoction has been used clinically for rheumatoid arthritis, its underlying anti-inflammatory mechanisms have not been systematically elucidated. Objectives: To systematically explore the anti-inflammatory mechanisms of Wenqing Bitong Decoction in rheumatoid arthritis using a network pharmacology approach. Materials and methods: Active compounds of the 14 Wenqing Bitong Decoction herbs were retrieved from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and HERB. TCMSP compounds were screened using OB ≥ 30% and DL ≥ 0.18; HERB compounds used a probability cutoff > 0.1 (SwissTargetPrediction, species Homo sapiens). Duplicates were removed. Rheumatoid arthritis targets from GeneCards (three-time median filtering, cutoff ≥ 5.71) and OMIM were intersected with drug targets. PPI was analyzed via STRING (Homo sapiens, confidence ≥ 0.7). GO/KEGG enrichment used adjusted p < 0.05. Results: A total of 183 bioactive compounds, 656 putative targets, and 867 rheumatoid arthritis-related targets were identified, yielding 93 overlapping targets. Network analysis indicated that key active compounds included quercetin, luteolin, kaempferol, wogonin, baicalein, and naringenin. Core targets such as IL6, IL1B, TNF, STAT3, and AKT1 were identified as central nodes in the PPI network. KEGG enrichment analysis revealed that these targets were mainly involved in TNF, IL-17, NF-κB, MAPK, PI3K-Akt, and JAK-STAT signaling pathways, which are closely associated with inflammatory response regulation and immune modulation. Conclusion: Wenqing Bitong Decoction may exert anti‑inflammatory effects in rheumatoid arthritis through multi‑component, multi‑target, and multi‑pathway mechanisms, potentially involving cytokine signaling modulation and key inflammatory pathways (NF‑κB, MAPK, PI3K‑Akt, JAK‑STAT). These findings are hypothesis‑generating and require experimental and clinical validation, as no validation was performed here.