Achyranthes bidentata polysaccharides induce chondrocyte proliferation via the promotion of the G1/S cell cycle transition

Mol Med Rep. 2013 Mar;7(3):935-40. doi: 10.3892/mmr.2013.1286. Epub 2013 Jan 22.

Abstract

Achyranthes bidentata polysaccharides (ABPS) are the major bioactive constituents of Radix Achyranthes bidentata (AB), which has been widely used in traditional Chinese medicine for the treatment of osteoarthritis. However, the molecular mechanisms behind the therapeutic effect of ABPS remain unclear. In the present study, chondrocytes were isolated from Sprague-Dawley rats. The effects of ABPS on the G1/S cell cycle transition in primary chondrocytes were investigated. The chondrocytes treated with and without ABPS were analyzed and it was observed that ABPS treatment was able to enhance chondrocyte proliferation in a dose- and time-dependent manner and promote the progression of chondrocyte cell cycle proliferation via the promotion of the G1 to S phase transition. Furthermore, using RT-PCR and western blot analysis, ABPS were observed as significantly upregulating the expression of cyclin D1 and the cyclin-dependent kinases (CDKs) CDK4 and CDK6. These results suggest that ABPS are able to promote chondrocyte proliferation via the promotion of the G1/S cell cycle transition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Achyranthes / chemistry
  • Animals
  • Cell Proliferation / drug effects*
  • Chondrocytes / cytology
  • Chondrocytes / drug effects*
  • Chondrocytes / metabolism
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism
  • Cyclin-Dependent Kinase 4 / genetics
  • Cyclin-Dependent Kinase 4 / metabolism
  • Cyclin-Dependent Kinase 6 / genetics
  • Cyclin-Dependent Kinase 6 / metabolism
  • G1 Phase / drug effects
  • Male
  • Polysaccharides / chemistry
  • Polysaccharides / pharmacology*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • S Phase / drug effects
  • Up-Regulation / drug effects

Substances

  • Polysaccharides
  • RNA, Messenger
  • Cyclin D1
  • Cyclin-Dependent Kinase 4
  • Cyclin-Dependent Kinase 6