4.7 Article

Chaenomeles Fructus (CF), the Fruit of Chaenomeles sinensis Alleviates IL-1β Induced Cartilage Degradation in Rat Articular Chondrocytes

期刊

出版社

MDPI
DOI: 10.3390/ijms23084360

关键词

osteoarthritis; Chaenomeles Fructus; Chaenomeles sinensis; cartilage degradation; natural product

资金

  1. Dongguk University Research Program
  2. National Research Foundation of Korea (NRF) - Korea government (MSIP) [NRF- 2020R1I1A3063625]

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This study demonstrates the anti-inflammatory and articular regeneration effects of Chaenomeles Fructus (CF) on rat chondrocytes with osteoarthritis, suggesting it as a promising therapeutic option for the treatment of OA.
Osteoarthritis (OA) causes persistent pain, joint dysfunction, and physical disability. It is the most prevalent type of degenerative arthritis, affecting millions of people worldwide. OA is currently treated with a focus on pain relief, inflammation control, and artificial joint surgery. Hence, a therapeutic agent capable of preventing or delaying the progression of OA is needed. OA is strongly associated with the degeneration of the articular cartilage and changes in the ECM, which are primarily associated with a decrease in proteoglycan and collagen. In the progress of articular cartilage degradation, catabolic enzymes, such as matrix metalloproteinases (MMPs), are activated by IL-1 beta stimulation. Given the tight relationship between IL-1 beta and ECM (extra-cellular matrix) degradation, this study examined the effects of Chaenomeles Fructus (CF) on IL-1 beta-induced OA in rat chondrocytes. The CF treatment reduced IL-1 beta-induced MMP3/13 and ADAMTS-5 production at the mRNA and protein levels. Similarly, CF enhanced col2a and aggrecan accumulation and chondrocyte proliferation. CF inhibited NF-kappa B (nuclear factor kappa B) activation, nuclear translocation induced by IL-1 beta, reactive oxygen species (ROS) production, and ERK phosphorylation. CF demonstrated anti-OA and articular regeneration effects on rat chondrocytes, thus, suggesting that CF is a viable and fundamental therapeutic option for OA.

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