Tanshinone IIA Induces Apoptosis in Fibroblast-Like Synoviocytes in Rheumatoid Arthritis <i>via</i> Blockade of the Cell Cycle in the G2/M Phase and a Mitochondrial Pathway

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  • Jie Ligang
    Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command HuaBo Bio-Pharmaceutic Institute of Guangzhou
  • Du Hongyan
    School of Biotechnology, Southern Medical University
  • Huang Qingchun
    Department of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine)
  • Wei Song
    Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command
  • Huang Runyue
    Department of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine)
  • Sun Weifeng
    Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command

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  • Tanshinone ⅡA Induces Apoptosis in Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via Blockade of the Cell Cycle in the G2/M Phase and a Mitochondrial Pathway

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Tanshinone IIA (Tan IIA), a phytochemical derived from the roots of Salvia miltiorrhiza BUNGE, has been documented with anti-tumor, pro-apoptotic, and anti-inflammatory activities. Salvia miltiorrhiza has long been used to treat rheumatoid arthritis (RA). Apoptosis induction of RA-fibroblast-like synoviocytes (FLS) was suggested to be a potential therapeutic approach for RA. The aim of this study was to investigate whether Tan IIA promotes apoptosis in RA-affected FLS. In this study, the viability of an immortalized FLS cell line derived from RA patients was assessed by 3-(4,5-dimethylthiazol-2-yl)-5,3-carboxymethoxyphenyl-2,4-sulfophenyl-2H-tetrazolium (MTS) assay after Tan IIA treatment. Apoptosis was measured by terminal deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL) assay and flow cytometry. Cell cycle was evaluated by flow cytometry. The expressions of mitochondrial apoptosis-related molecules, including Bcl-2, Bax, mitochondrial cytochrome c (Cyt-c), cytosolic Cyt-c, apoptotic protease activating factor 1 (Apaf-1), procaspase-9, procaspase-3, caspase-9, and caspase-3 were determined by Western blotting. Our data demonstrate that Tan IIA induced apoptosis of RA-FLS, blocked the cell cycle in the G2/M phase, and regulated the protein expression of Bcl-2, Bax, and Apaf-1, the release of mitochondrial Cyt-c, and the activation of caspase-9 and caspase-3. The results support the conclusion Tan IIA treatment likely induces apoptosis of RA-FLS through blockade of the cell cycle in the G2/M phase and a mitochondrial pathway. These data suggest that Tan IIA may have therapeutic potential for RA.

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