scholarly journals Chondroprotective Effects and Multitarget Mechanisms of Fu Yuan Capsule in a Rat Osteoarthritis Model

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Li Zeng ◽  
Cai Zhi Xiao ◽  
Zi Ting Deng ◽  
Rong Heng Li
Keyword(s):  
Articular Cartilage ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Type Ii Collagen ◽  
Pharmacological Mechanism ◽  
Articular Cartilage Injury ◽  
Anterior Cruciate ◽  
A Disintegrin And Metalloproteinase

Fu Yuan Capsule (FYC) has been clinically used for osteoarthritis (OA) and its related diseases for many years in China. However, its pharmacological mechanism remains unclear. This study aimed to investigate the potential chondroprotective effects of FYC on articular cartilage. Rat OA model was induced by anterior cruciate ligament transection. A group of rats was treated with FYC for 12 weeks. Joint structure, types I and II collagen, and proteoglycan were evaluated by histological examination. The expression of C-terminal crosslinking telopeptide of type II collagen, hydroxyproline, a disintegrin and metalloproteinase with thrombospondin motifs, matrix metalloproteinase, interleukin-1 beta, nitric oxide, prostaglandin E2, heat-shock protein 70, transforming growth factor-beta, osteoprotegerin, and receptor activator of nuclear factor κB ligand were detected. Treatment with FYC could protect against articular cartilage injury. FYC treatment significantly decreased the extracellular matrix degradation factors and inflammatory mediators. Moreover, articular cartilage protective factors were increased in the FYC group. The current finding suggests that FYC protects articular cartilage in a rat OA model through various ways. Thus, it may be an effective agent for OA treatment.

scholarly journals Melatonin Prevents Osteoarthritis-Induced Cartilage Degradation via Targeting MicroRNA-140

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Yijian Zhang ◽  
Jun Lin ◽  
Xinfeng Zhou ◽  
Xi Chen ◽  
Angela Carley Chen ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Interleukin 1 ◽  
Type Ii Collagen ◽  
Cartilage Degradation ◽  
A Disintegrin And Metalloproteinase ◽  
Surgically Induced ◽  
Metalloproteinase 9 ◽  
Synthesis And Degradation

Osteoarthritis (OA) is characterized by the progressive destruction of articular cartilage, which is involved in the imbalance between extracellular matrix (ECM) synthesis and degradation. MicroRNA-140-5p (miR-140) is specifically expressed in cartilage and plays an important role in OA-induced matrix degradation. The aim of this study was to investigate (1) whether intra-articular injection of melatonin could ameliorate surgically induced OA in mice and (2) whether melatonin could regulate matrix-degrading enzymes at the posttranscriptional level by targeting miR-140. In an in vitro OA environment induced by interleukin-1 beta (IL-1β), melatonin treatment improved cell proliferation of human chondrocytes, promoted the expression of cartilage ECM proteins (e.g., type II collagen and aggrecan), and inhibited the levels of IL-1β-induced proteinases, such as matrix metalloproteinase 9 (MMP9), MMP13, ADAMTS4 (a disintegrin and metalloproteinase with thrombospondin motifs 4), and ADAMTS5. Both the microarray and polymerase chain reaction (PCR) experiments revealed that miR-140 was a melatonin-responsive microRNA and melatonin upregulated miR-140 expression, which was suppressed by IL-1β stimulation. In vivo experiments demonstrated that intra-articular injection of melatonin prevented disruptions of cartilage matrix homeostasis and successfully alleviated the progression of surgery-induced OA in mice. Transfection of miR-140 antagomir completely counteracted the antiarthritic effects of melatonin by promoting matrix destruction. Our findings demonstrate that melatonin protects the articular cartilage from OA-induced degradation by targeting miR-140, and intra-articular administration of melatonin may benefit patients suffering from OA.

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