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Volume 30, Issue 1, Pages 57-65 (January 2010)


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Icariin protects murine chondrocytes from lipopolysaccharide-induced inflammatory responses and extracellular matrix degradation

Man-Hai Liub, Jui-Sheng SunacCorresponding Author Informationemail addressemail address, Shaio-Wen Tsaib, Shiow-Yunn SheubCorresponding Author Informationemail address, Ming-Hong Chend

Received 25 August 2009; received in revised form 28 September 2009; accepted 21 October 2009.

Abstract 

Septic arthritis is an inflammatory arthropathy characterized by degeneration of articular cartilage. Icariin, the main active flavonoid glucoside isolated from Epimedium pubescens, is used as antirheumatics (or antiinflammatory), tonics, and aphrodisiacs in traditional Chinese medicine. In this study, we used lipopolysaccharide (LPS) to simulate the in vitro inflammatory response of chondrocytes during septic arthritis. Our hypothesis is that the icariin can protect chondrocytes from LPS-induced inflammation and extracellular matrix degradation. The inflammation of neonatal mice chondrocytes was induced by LPS and the antiinflammatory effects were examined. The synthesis of nitric oxide was analyzed, whereas the titer of glycosaminoglycan and total collagen were measured and the gene expressions (including inducible nitric oxide synthase [iNOS], matrix metalloproteinase [MMP]–1, MMP-3, and MMP-13) were evaluated. The results showed that the viability of chondrocytes, extracellular matrix synthesis, was significantly decreased, whereas nitric oxide synthesis was significantly increased in the presence of 10−5 g/mL LPS. Icariin pretreatment can partially reverse these effects. The up-regulated expressions of MMP-1, 3, 13, cyclooxygenase-2 (COX-2), and iNOS genes by LPS treatment were also significantly down-regulated by the pretreatment of icariin to 1.8%, 0.056%, 7.7%, 3.1%, and 5.3% of the LPS-positive control sample, respectively. Our results demonstrate that icariin is a safe anabolic agent of chondrocytes. Icariin may exert its protective effects through inhibition of nitric oxide and MMP synthesis, and may then reduce the extracellular matrix destruction.

a Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei City 11031, Taiwan, ROC

b School of Pharmacy, Taipei Medical University, Sinyi District, Taipei City 110, Taiwan, ROC

c Department of Orthopedic Surgery, Taipei Medical University- Shuang Ho Hospital, Jhonghe City, Taipei County 235, Taiwan, ROC

d Institute of Biomedical Engineering, National Yang-Ming University, Taipei, Taiwan, R.O.C.

Corresponding Author InformationCorresponding authors. Jui-Sheng Sun is to be contacted at Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei City 11031, Taiwan, ROC, and Department of Orthopedic Surgery, Taipei Medical University- Shuang Ho Hospital, Jhonghe City, Taipei County 235, Taiwan, ROC. Tel.: +886 2 27361661x3229, +886 2 22490088; fax: +886 2 27390500. Or Shiow-Yunn Sheu, School of Pharmacology, College of Pharmacy, Taipei Medical University, Taipei City 11031, Taiwan, ROC.

PII: S0271-5317(09)00205-X

doi:10.1016/j.nutres.2009.10.020


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