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Isorhapontigenin Suppresses Interleukin-1β-Induced Inflammation and Cartilage Matrix Damage in Rat Chondrocytes

  • Yongzhuang Ma
  • Chang Tu
  • Wei Liu
  • Yifan XiaoEmail author
  • Hua WuEmail author
Original Article
  • 25 Downloads

Abstract

Osteoarthritis (OA) is a common cause of joint pain and physical disability in the elderly. It is highly associated with local inflammatory reactions and cartilage degradation. Isorhapontigenin (ISO), a natural compound existing in various plants, has shown prominent anti-inflammatory and anti-oxidative properties in several inflammatory diseases. However, the effects of ISO on OA remain to be elucidated. Here, we investigated the effects of ISO on interleukin-1β (IL-1β)-treated rat chondrocytes and cartilage explants. Our results revealed that ISO could suppress the IL-1β-induced elevated levels of nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), and cyclooxygenase-2 (COX2). Besides, ISO could also inhibit the IL-1β-induced up-regulation of cartilage matrix catabolic enzymes such as matrix metalloproteinases (MMPs) and aggrecanase-2 (ADAMTS5). Moreover, the IL-1β-induced downregulation of collagen II and aggrecan could be reversed by ISO. Furthermore, ISO prevented rat cartilage explant damage induced by IL-1β. Mechanistically, ISO worked partly by suppressing mitogen-activated protein kinase (MAPK)-associated ERK and p38 pathways. Taken together, our study indicated the anti-inflammatory potential of ISO on IL-1β-treated rat chondrocytes, providing a new idea for OA treatment.

KEY WORDS

osteoarthritis isorhapontigenin iNOS COX2 MMPs ADAMTS5 

Notes

Acknowledgments

This study was supported by the grant from the National Natural Science Foundation of China (no. 51537004) to H.W.

Compliance with Ethical Standards

This study was in strict accordance with the Guidelines of Animal Care and Use Committee for Teaching and Research of Huazhong University of Science and Technology, Wuhan, China.

Conflict of Interest

The authors have no conflict of interest or financial disclosures with this research.

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© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  1. 1.Department of Orthopedics, Tongji HospitalTongji Medical College, Huazhong University of Science and TechnologyWuhanPeople’s Republic of China
  2. 2.Department of Pathology and Pathophysiology, School of MedicineJianghan UniversityWuhanPeople’s Republic of China

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