2. Academic Validation
  3. Dopamine delays articular cartilage degradation in osteoarthritis by negative regulation of the NF-κB and JAK2/STAT3 signaling pathways

Dopamine delays articular cartilage degradation in osteoarthritis by negative regulation of the NF-κB and JAK2/STAT3 signaling pathways

  • Biomed Pharmacother. 2019 Nov;119:109419. doi: 10.1016/j.biopha.2019.109419.
Wei Lu 1,  Zhenfei Ding 1,  Fuen Liu 1,  Wenshan Shan 1,  Chao Cheng 2,  Jiegou Xu 3,  Wei He 3,  Wei Huang 4,  Junting Ma 5,  Zongsheng Yin 6
Affiliations

Affiliations

  • 1 Department of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, 218#Ji Xi Road, Hefei, 230032, Anhui, China.
  • 2 Department of Orthopaedics, The Fourth Affiliated Hospital of Anhui Medical University, 372#Tun Xi Road, Hefei, 230032, Anhui, China.
  • 3 School of Basic Medical Sciences, Anhui Medical University, 81#Mei Shan Road, Hefei, 230032, Anhui, China.
  • 4 Department of Orthopaedics, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, 17#Lu Jiang Road, Hefei, 230001, Anhui, China. Electronic address: ahslyyhwei@126.com.
  • 5 School of Basic Medical Sciences, Anhui Medical University, 81#Mei Shan Road, Hefei, 230032, Anhui, China. Electronic address: majunting@ahmu.edu.cn.
  • 6 Department of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, 218#Ji Xi Road, Hefei, 230032, Anhui, China. Electronic address: anhuiyzs@126.com.
PMID: 31563117 DOI: 10.1016/j.biopha.2019.109419
Abstract

Background: The progressive loss of cartilage matrix and the breakdown of articular cartilage induced by inflammation play an essential role in osteoarthritis (OA) pathogenesis. Dopamine (DA) is a critical neurotransmitter that is not only involved in controlling exercise, emotion, cognition and neuroendocrine activity but also has anti-inflammatory effects. This study aimed to investigate the effects of DA on OA in vitro and in vivo.

Methods: OA progression was evaluated in a mouse model with surgically induced destabilization of the medial meniscus. Cartilage degradation and OA were analyzed using Safranin O/Fast Green staining. Additionally, qRT-PCR and Western blotting were applied to detect catabolic and anabolic factors involved in cartilage degeneration and underlying mechanisms in OA chondrocytes treated with Interleukin-1β.

Results: In vitro, DA treatment inhibited the production of inducible nitric oxide synthase, cyclooxygenase-2, matrix metalloproteinase (MMP)-1, MMP-3, and MMP-13, while increasing type II collagen and glycosaminoglycan content. Mechanistically, DA reversed IL-1β-treated nuclear factor-kappa B activation and JAK2/STAT3 phosphorylation. Furthermore, DA suppressed the degradation of cartilage matrix and reduced Osteoarthritis Research Society International scores in the surgically induced OA models.

Conclusion: DA may be a novel therapeutic agent for OA treatment.

Keywords

Chondrocytes; Dopamine; JAK2/STAT3; NF-κB; Osteoarthritis.

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