title: Ginsenoside Rb1 prevents interleukin-1 beta induced inflammation and apoptosis in human articular chondrocytes.
abstract: OBJECTIVE
  Osteoarthritis (OA) is an age-related joint disease that is characterised by the degeneration of articular chondrocytes. Ginsenosides, the most important pharmacological ingredients of ginseng, have been proven to provide effective therapy for neurodegenerative diseases and can inhibit cell apoptosis. We investigated whether ginsenoside Rb1 can modulate inflammation and apoptosis in human chondrocytes.
  
  
  METHODS
  Chondrocytes were isolated from OA patients undergoing total knee replacement surgery. Apoptosis was assessed by TUNEL (terminal deoxyribonucleotide transferasemediated dUTP nick end-labelling)-positive staining. Levels of PGE2 and NO(2)- were detected by ELISA. Gene expression levels were measured for type II collagen (Col2A1), aggrecan, MMP-13, COX-2, iNOS, caspase-3, and PARP.
  
  
  RESULTS
  The results showed that TUNEL-positive staining chondrocytes were decreased by Rb1 compared with IL-1β. Both 10 or 100 μg/ml Rb1 inhibited the effect of IL-1β on chondrocytes by decreasing levels of PGE2, NO(2)-, MMP-13, COX-2, iNOS, caspase-3 and PARP and increasing aggrecan and Col2A1 gene expression levels, to block IL-1β-induced cell inflammation and apoptosis.
  
  
  CONCLUSIONS
  The results suggest that Rb1 possesses potential anti-inflammatory and anti-apoptotic properties in human chondrocytes, possibly by binding to oestrogen receptors to exert its pharmacological effects.
authors.affiliation: Department of Orthopedics, The First Affiliated Hospital of Nanjing Medical University, 300 Guang Zhou Road, Nanjing, 210000, China.
authors.forename: Wendan
authors.initials: W
authors.lastname: Cheng
authors.forename: Dongying
authors.initials: D
authors.lastname: Wu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Zuo
authors.forename: Zhen
authors.initials: Z
authors.lastname: Wang
authors.forename: Weimin
authors.initials: W
authors.lastname: Fan
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D002358:Cartilage, Articular / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D002478:Cells, Cultured; D019902:Chondrocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D036145:Ginsenosides / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D007249:Inflammation / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D053583:Interleukin-1beta / Q000009:adverse effects*; D053509:Matrix Metalloproteinase 13 / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism
chemical_list: D036145:Ginsenosides; D053583:Interleukin-1beta; D009573:Nitrites; C442759:ginsenoside Rb1; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D053148:Caspase 3; D053509:Matrix Metalloproteinase 13; D015232:Dinoprostone