Research Paper Volume 12, Issue 17 pp 17137—17149
The protective effects of dehydrocostus lactone against TNF-α-induced degeneration of extracellular matrix (ECM) in SW1353 cells
- 1 Department of Orthopaedics, Yijishan Hospital of Wannan Medical College, Wuhu 241000, Anhui Province, China
- 2 Department of Orthopaedics, The Fourth Affiliated Hospital of Anhui Medical University, Hefei 230012, Anhui Province, China
Received: April 14, 2020 Accepted: June 22, 2020 Published: September 14, 2020https://doi.org/10.18632/aging.103657
How to Cite
Copyright: © 2020 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Osteoarthritis is a common joint disease that disrupts the lives of millions of people worldwide. To date, a safe and reliable treatment has not yet been announced. Excessive production of pro-inflammatory cytokines such as TNF-α plays an important role in the pathological development of OA. Dehydrocostus lactone (DHC) is a kind of sesquiterpene isolated from medicinal plants that has been demonstrated to play a protective role in inflammation and tumor formation. However, the effects of DHC in OA hasn’t been reported before. In the present study, we investigated the antioxidant and protective effects of DHC in human chondrocytes against insult from tumor necrosis factor-α (TNF-α). We found that DHC inhibited oxidative stress by suppressing the production of reactive oxygen species (ROS) from TNF-α stimulation. Furthermore, DHC decreased the expression of pro-inflammatory cytokines induced by TNF-α, such as interleukin-1β (IL-1β) and interleukin-6 (IL-6). Importantly, DHC prevented the degradation of type II collagen and aggrecan, which are the main components of the extracellular matrix (ECM), by inhibiting the overexpression of matrix metalloproteinases (MMPs) and a disintegrin and metalloproteinase with a thrombospondin type 1 motif (ADAMTS) induced by TNF-α. Mechanistically, DHC ameliorated the inflammatory response and degeneration of the articular extracellular matrix (ECM) by suppressing nuclear factor-κB (NF-κB) activation. Our results reveal that DHC possesses a beneficial effect against TNF-α-mediated insult in human chondrocytes, implying a potential role for DHC in the treatment of osteoarthritis (OA).