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Letter

Response to 'TNF/TNFR signal transduction pathway-mediated anti-apoptosis and anti-inflammatory effects of sodium ferulate on IL-1β-induced rat osteoarthritis chondrocytes in vitro'

Jing Ma1, Ang Li1, Shu Zhu2, Xiao-Rui Cao2 and Guo-Xian Pei2*

Author Affiliations

1 School of Stomatology, Fourth Military Medical University, 15 Changle Western Road, Xi'an 710032, PR China

2 Department of Orthopaedics, Xijing Hospital, 127 Changle Western Road, Fourth Military Medical University, Xi'an 710032, PR China

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Arthritis Research & Therapy 2013, 15:408  doi:10.1186/ar4226


See related research by Qin et al., http://arthritis-research.com/content/14/6/R242, and related letter by Qin et al., http://arthritis-research.com/content/15/3/409

Published: 24 May 2013

First paragraph (this article has no abstract)

We read with great interest the research article by Qin and colleagues, in which they addressed, on the basis of their previous work, the underlying mechanisms for the protective effect of a small component of traditional Chinese herbs, sodium ferulate (SF), on osteoarthritis (OA) [1]. Utilizing the classical in vitro OA chondrocyte model induced by IL-1β, they provided lines of evidence that SF does make a big difference to the OA model in a dose-dependent manner. Furthermore, the underlying mechanisms of the effects were owing to the regulative role of SF on the apoptotic machinery. However, we would like to supplement as well as applaud the authors' findings with particular reference to the apoptotic machinery regulation.