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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- Jie Ligang
- Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command HuaBo Bio-Pharmaceutic Institute of Guangzhou
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- Du Hongyan
- School of Biotechnology, Southern Medical University
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- Huang Qingchun
- Department of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine)
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- Wei Song
- Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command
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- Huang Runyue
- Department of Rheumatology, The Second Affiliated Hospital, Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine)
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- Sun Weifeng
- Department of Chinese Medicine, Guangzhou General Hospital of Guangzhou Command
書誌事項
- タイトル別名
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- 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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抄録
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.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 37 (8), 1366-1372, 2014
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679611073792
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- NII論文ID
- 130004057436
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC2cfhtlOnsg%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 025610158
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- PubMed
- 24920239
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可