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Cited by 85Natural Compounds in Disease TreatmentRheumatoid Arthritis Research and TherapiesOsteoarthritis Treatment and Mechanisms

Madecassoside attenuates inflammatory response on collagen-induced arthritis in DBA/1 mice

Li, Hongzhong, Gong, Xia, Zhang, Li, Zhang, Zhuo, Luo, Fuling, Zhou, Qixin, Chen, Jin, Wan, Jingyuan·2009·Phytomedicine
DOI 10.1016/j.phymed.2008.11.002
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Abstract

Madecassoside (MA), a triterpenoid product isolated from Centella asiatica, has been described to exhibit antioxidant and anti-inflammatory activities. The present study was undertaken to determine whether madecassoside (MA) is efficacious against collagen-induced arthritis (CIA) in mice and its possible mechanisms. DBA/1J mice were immunized with bovine type II collagen and treated with MA (3, 10 and 30 mg/kg d, i.g.) from days 21 to 42 after immunization. Arthritis was evaluated by hind paw swelling, polyarthritis index, and histological examination. In vitro proliferation of spleen cells was examined using 3-[4,5-dimethylthylthiazol-2-yl]-2, 5-diphenyltetrazoliumbromide (MTT) assay. Plasma levels of cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-10 (IL-10) and the expression of prostaglandin E(2) (PGE(2)), cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in synovial tissues were also determined. The results showed that comparing with untreated CIA mice, treated with MA dose-dependently suppressed the clinical arthritis score and joints tissues pathological damage, reduced the proliferation of spleen cells, plasma levels of TNF-alpha and IL-6, synovial tissues PGE(2) production and COX-2 protein expression, however, the expression of COX-1 in synovial tissues did not change and the plasma levels of IL-10 were increased. These results suggest that MA can effectively alleviate inflammatory response on CIA, and anti-inflammatory effec…

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  • Madecassoside-treated arthritic mice showed improvement in pathological damage to joint tissues, significant suppression of pro-inflammatory molecules COX-2, PGE(2), TNF-alpha and IL-6, as well as upregulation of anti-inflammatory mediator IL-10.

    “the madecassoside‐treated arthritic mice showed improvement in the pathological damage to joint tissues, significant suppression of the pro‐inflammatory molecules COX‐2, PGE (2), TNF‐alpha and IL‐6, as well as upregulation of the anti‐inflammatory mediator IL‐10.”

    From Therapeutic Properties and Pharmacological Activities of Asiaticoside and Madecassoside: A Review (2023) · cites this paper as [134]

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Authors
Li, H., Gong, X., Zhang, L., Zhang, Z., Luo, F., Zhou, Q., Chen, J., & Wan, J.
Affiliations
  • Chongqing Medical University (CN)
  • Second Affiliated Hospital of Chongqing Medical University (CN)
Corresponding author
Wan, Jingyuan
ORCID
Venue
Phytomedicine
Publisher
Elsevier BV
Published
2009-06
Volume
16
Issue
6-7
Pages
538-546
ISSN
0944-7113 (ISSN-L)
DOI
10.1016/j.phymed.2008.11.002
OpenAlex
W1999586472
Cited by
85
References
2
Citations by year
2026: 1 · 2025: 5 · 2024: 5 · 2023: 5 · 2022: 2 · 2021: 4 · 2020: 9 · 2019: 8 · 2018: 6 · 2017: 2 · 2016: 5 · 2015: 5 · 2014: 9 · 2013: 6 · 2012: 4
FWCI
10.60
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Phytomedicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Health Sciences › Medicine › Complementary and alternative medicine › Natural Compounds in Disease Treatment
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
  • Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
Keywords
madecassoside, Centella asiatica, collagen-induced arthritis, anti-inflammatory activity, triterpenoids, cyclooxygenase-2, prostaglandin E2, TNF-α, interleukin-6, IL-10, synovium, spleen cell proliferation, DBA/1J mice
MeSH terms
Animals, Arthritis, Experimental, Inflammation, Male, Mice, Inbred DBA, Synovial Membrane, Triterpenes, Blotting, Western, Dinoprostone, Cytokines, Inflammation Mediators, Cell Proliferation, Mice

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