How Ginseng Compounds Help Reduce Blood Vessel Growth in Rheumatoid Arthritis

Jenn Hoskins
6th June, 2024

How Ginseng Compounds Help Reduce Blood Vessel Growth in Rheumatoid Arthritis

Image Source: Natural Science News, 2024

Key Findings

  • The study by China Three Gorges University investigated the effects of Panax japonicus C.A. Meyer on rheumatoid arthritis (RA)
  • Researchers found that total saponins of Panax japonicus (TSPJs) can inhibit the formation of new blood vessels in RA
  • TSPJs work by targeting key proteins involved in angiogenesis, reducing inflammation, and preventing joint damage
Rheumatoid arthritis (RA) is a chronic inflammatory disorder that primarily affects joints, leading to pain, swelling, and eventually joint destruction. One critical factor in RA progression is angiogenesis, the formation of new blood vessels, which supplies nutrients and inflammatory cells to the synovial membrane, exacerbating the disease. Traditional Chinese herbal medicine, particularly Panax japonicus C.A. Meyer, has been employed in RA treatment for centuries, but the mechanisms behind its efficacy remain largely unexplored. A recent study by researchers at China Three Gorges University aims to shed light on this by investigating the effects of total saponins of Panax japonicus C.A. Meyer (TSPJs) on synovial angiogenesis in RA[1]. The study utilized network pharmacology and bioinformatics to predict the potential targets and mechanisms of TSPJs in RA treatment. The results suggested that TSPJs might inhibit RA-related angiogenesis through the hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) pathways. To validate these predictions, the researchers conducted both in vitro and in vivo experiments. In vitro experiments demonstrated that different doses of TSPJs effectively inhibited tube formation in EA.hy926 cells, a model for human vascular endothelial cells. The cellular thermal shift assay further indicated that TSPJs could bind to key proteins involved in angiogenesis, such as HIF-1α, VEGFA, and angiopoietin-1 (ANG-1). These findings align with previous research showing that targeting the HIF-VEGF-Ang axis can significantly impact RA progression[2]. In vivo, the study used a collagen-induced arthritis (CIA) mouse model to evaluate the therapeutic effects of TSPJs. The administration of TSPJs alleviated RA symptoms, including reduced arthritis index, hind paw thickness, and swollen joint count. Histological analysis revealed that TSPJs inhibited inflammation, angiogenesis, bone damage, and cartilage destruction. The number of blood vessels and the expression level of CD31, a marker for angiogenesis, were also significantly decreased in the TSPJ-treated mice. The mechanistic results showed that TSPJs reduced the expression levels of HIF-1α, VEGFA, and ANG-1 in the serum or synovial tissues of CIA mice. This suggests that the anti-angiogenic effects of TSPJs are mediated through the inhibition of the HIF-1α/VEGF/ANG-1 axis. This finding is particularly significant as it builds upon earlier studies that identified these pathways as crucial in RA pathogenesis[3]. Previous research has also highlighted the importance of angiogenesis in RA and explored various compounds for their anti-angiogenic properties. For instance, matrine (Mat) has been shown to exert anti-angiogenic effects by regulating the HIF-VEGF-Ang axis and inhibiting the PI3K/Akt signaling pathway, thereby improving RA symptoms[2]. Similarly, genistein (GEN), a soy-derived isoflavone, has been found to inhibit VEGF expression and angiogenesis through the JAK2/STAT3 pathway, providing another potential therapeutic avenue for RA[4]. Interestingly, the study also aligns with findings on the role of the adipokine apelin (APLN) in RA. APLN facilitates angiogenesis by increasing ANG-1 expression and inhibiting miR-525-5p synthesis via PLCγ and PKCα signaling. Targeting APLN has shown promise in mitigating angiogenesis and RA symptoms[5]. The current study on TSPJs adds another layer to this understanding by demonstrating a different yet complementary mechanism involving the HIF-1α/VEGF/ANG-1 axis. In conclusion, the study by China Three Gorges University provides compelling evidence that TSPJs can effectively inhibit angiogenesis in RA by targeting the HIF-1α/VEGF/ANG-1 axis. This research not only validates the traditional use of Panax japonicus C.A. Meyer in RA treatment but also offers a potential new therapeutic strategy for managing this debilitating disease. The findings integrate well with previous studies, collectively advancing our understanding of the complex mechanisms driving RA and highlighting new avenues for therapeutic intervention.



Main Study

1) The antiangiogenic effect of total saponins of Panax japonicus C.A. Meyer in rheumatoid arthritis is mediated by targeting the HIF-1α/VEGF/ANG-1 axis.

Published 3rd June, 2024

Related Studies

2) Matrine inhibits synovial angiogenesis in collagen-induced arthritis rats by regulating HIF-VEGF-Ang and inhibiting the PI3K/Akt signaling pathway.

3) The non-major histocompatibility complex quantitative trait locus Cia10 contains a major arthritis gene and regulates disease severity, pannus formation, and joint damage.

Journal: Arthritis and rheumatism, Issue: Vol 52, Issue 1, Jan 2005

4) Genistein inhibits angiogenesis developed during rheumatoid arthritis through the IL-6/JAK2/STAT3/VEGF signalling pathway.

5) Apelin Promotes Endothelial Progenitor Cell Angiogenesis in Rheumatoid Arthritis Disease via the miR-525-5p/Angiopoietin-1 Pathway.

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