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

Int J Mol Sci. 2022 Apr 14;23(8):4360. doi: 10.3390/ijms23084360.

Abstract

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-1β stimulation. Given the tight relationship between IL-1β and ECM (extra-cellular matrix) degradation, this study examined the effects of Chaenomeles Fructus (CF) on IL-1β-induced OA in rat chondrocytes. The CF treatment reduced IL-1β-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-κB (nuclear factor kappa B) activation, nuclear translocation induced by IL-1β, 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.

Keywords: Chaenomeles Fructus; Chaenomeles sinensis; cartilage degradation; natural product; osteoarthritis.

MeSH terms

  • Animals
  • Cartilage, Articular* / metabolism
  • Cells, Cultured
  • Chondrocytes / metabolism
  • Fruit / metabolism
  • Humans
  • Interleukin-1beta / pharmacology
  • Interleukin-1beta / therapeutic use
  • NF-kappa B / metabolism
  • Osteoarthritis* / metabolism
  • Rats
  • Rosaceae* / metabolism
  • Signal Transduction

Substances

  • Interleukin-1beta
  • NF-kappa B