AI Article Synopsis
- Naru-3 is a traditional Mongolian medicine used to treat rheumatoid arthritis (RA) and is made from three key herbs: Aconitum kusnezoffii, Terminalia chebula, and Piper longum, which have a long history of use in the region.
- The study investigated Naru-3's effectiveness using a rat model of collagen-induced arthritis, comparing its effects to those of Etanercept (ETN) over four weeks, focusing on various physical symptoms and inflammation markers.
- Results showed that Naru-3 significantly reduced symptoms such as paw swelling, inhibited inflammation and neovascularization, and was more effective in preventing neovascularization compared to ETN, indicating its potential as a treatment for RA
Article Abstract
Ethnopharmacological Relevance: Naru-3 is a prescribed formulation based on the theory of Mongolian medicine for the treatment of rheumatoid arthritis (RA). Naru-3 consists of three medicinal agents: Aconitum kusnezoffii Reichb (caowu), Terminalia chebula Retz (hezi), and Piper longum L (biba). These medicinal agents are widely distributed in the Mongolian area of China and have been used to treat rheumatism for centuries.
Background: Mongolian medicine Naru-3 is commonly prescribed to treat RA, but its mechanism of action is unknown.
Methods: A rat collagen-induced arthritis (CIA) model was established to investigate the mechanism of Naru-3. Rats were treated with Naru-3, Etanercept (ETN), and sodium carboxymethylcellulose (CMC) for four weeks. After treatment was terminated, paw thickness, ankle diameter, and arthritis index (AI) were scored. Synovial hyperplasia was evaluated using hematoxylin and eosin (H&E) staining and two-dimensional ultrasonography. Synovitis and neovascularization were assayed using power Doppler imaging (PDI) and contrast-enhanced ultrasonography (CEUS). Levels of vascular endothelial growth factor (VEGF), interleukin (IL)-1, and CD31 in the serum or synovium were detected using ELISA and immunohistochemistry analyses.
Results: Naru-3 and ETN alleviated the symptoms of CIA as evidenced by diminished paw thickness, ankle diameter, and AI scores. Mechanistically, Naru-3 inhibited synovial hyperplasia, synovitis, and neovascularization by diminishing systemic and local inflammation, as indicated by the relative expression of CD31, VEGF and IL-1 in the serumor synovium. After four weeks of treatment, no significant neovascularization was observed in the Naru-3 group, but neovascularization and synovitis occurred in the ETN group, as demonstrated by H&E staining, PDI, and CEUS examination.
Conclusion: Naru-3 inhibited inflammation, synovial hyperplasia, and neovascularization and alleviates RA in our CIA rat model. No symptom recurrence was observed four weeks after drug treatment.
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| http://dx.doi.org/10.1016/j.jep.2023.116350 | DOI Listing |
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