title: Salvianolic acid B regulates gene expression and promotes cell viability in chondrocytes.
abstract: Articular chondrocytes reside in lacunae distributed in cartilage responsible for the remodelling of the tissue with limited ability of damage repairing. The in vitro expanded chondrocytes enhanced by factors/agents to obtain large numbers of cells with strengthened phenotype are essential for successful repair of cartilage lesions by clinical cell implantation therapies. Because the salvianolic acid B (Sal B), a major hydrophilic therapeutic agent isolated from Salvia miltiorrhiza, has been widely used to treat diseases and able to stimulate activity of cells, this study examines the effects of Sal B on passaged chondrocytes. Chondrocytes were treated with various concentrations of Sal B in monolayer culture, their morphological properties and changes, and mitochondrial membrane potential were analysed using microscopic analyses, including cellular biochemical staining and confocal laser scanning microscopy. The proteins were quantified by BCA and Western blotting, and the transcription of genes was detected by qRT-PCR. The passaged chondrocytes treated with Sal B showed strengthened cellular synthesis and stabilized mitochondrial membrane potential with upregulated expression of the marker genes for chondrocyte phenotype, Col2-α1, Acan and Sox9, the key Wnt signalling molecule β-catenin and paracrine cytokine Cytl-1. The treatments using CYTL-1 protein significantly increased expression of Col2-α1 and Acan with no effect on Sox9, indicating the paracrine cytokine acts on chondrocytes independent of SOX9. Sal B has ultimately promoted cell growth and enhanced chondrocyte phenotype. The chondrocytes treated with pharmaceutical agent and cytokine in the formulated medium for generating large number of differentiated chondrocytes would facilitate the cell-based therapies for cartilage repair.
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Yang
authors.affiliation: Department of General Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Shaojie
authors.initials: S
authors.lastname: Liu
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Siming
authors.initials: S
authors.lastname: Li
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Pengzhen
authors.initials: P
authors.lastname: Wang
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Weicong
authors.initials: W
authors.lastname: Zhu
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Peihong
authors.initials: P
authors.lastname: Liang
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.
authors.forename: Jianrong
authors.initials: J
authors.lastname: Tan
authors.affiliation: Guangzhou Institute of Traumatic Surgery, Guangzhou Red Cross Hospital, Jinan University School of Medicine, Guangzhou, China.|Department of Zoology, Faculty of Science, the University of Melbourne, Parkville, Victoria, Australia.
authors.forename: Shuliang
authors.initials: S
authors.lastname: Cui
mesh_terms: D053674:Aggrecans / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001572:Benzofurans / Q000494:pharmacology*; D049109:Cell Proliferation / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D002478:Cells, Cultured; D019902:Chondrocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D024043:Collagen Type II / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects*; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D009696:Nucleic Acids / Q000096:biosynthesis; D011817:Rabbits; D018121:Receptors, Cytokine / Q000378:metabolism; D055758:SOX9 Transcription Factor / Q000235:genetics / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects; D053630:Depsides
chemical_list: D053674:Aggrecans; D001572:Benzofurans; D024043:Collagen Type II; D009696:Nucleic Acids; D018121:Receptors, Cytokine; D055758:SOX9 Transcription Factor; C113554:cytokine-like factor-1; C076944:salvianolic acid B; D053630:Depsides
keywords: 
  Cytl-1
  ; 
  Sox9
  ; chondrocyte activity; collagen type I (COL I); collagen type II (COL II); passaged chondrocytes; salvianolic acid B; viable cells; β-catenin