Bcl-2 Family Proteins Were Involved in Pseudolaric Acid B-Induced Autophagy in Murine Fibrosarcoma L929 Cells
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概要
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Pseudolaric acid B (PAB) exerted cytostatic activity on murine fibrosarcoma L929 cells. The cytostatic mechanism of PAB on L929 cells was investigated in this paper. At 36 h, after 80 μM PAB treatment, the inhibitory ratio was 65.37 ± 4.12%, and the MDC staining ratio was strongest in L929 cells. 3-Methyladenine (3-MA), an inhibitor of autophagy, inhibited the generation of autolysosomes induced by PAB. The expression of autophagy-associated Beclin 1 protein was up-regulated, and microtubule-associated protein light chain 3 I (LC3 I) was cleaved into LC3 II after 80 μM PAB treatment from 12 h. Therefore, it was concluded that PAB exerted a cytostatic effect on L929 cells through autophagy. However, 80 μM PAB treatment did not induce apoptotic body formation, but 3 mM 3-MA promoted apoptosis, so autophagy might inhibit apoptosis. PAB had no effect on mitochondrial membrane potential (MMP), but up-regulated the expressions of Bax and Bcl-2. Immunoprecipitation analysis showed that PAB inhibited Bcl-2 binding with Beclin 1. Additionally, PAB inhibited the localization of Bax in mitochondria, but Bcl-2 still was in the mitochondria to sustain MMP. Meanwhile PAB promoted the phosphorylation of cytoplasmic Bcl-2. Therefore the phosphorylation of Bcl-2 in the cytoplasm and the mitochondrial location of Bcl-2 might be the reasons why PAB inhibited the binding of Bcl-2 and Beclin 1.
- 2008-07-20
著者
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Tashiro Shin-ichi
Dep. Of Clinical And Biomedical Sciences Showa Pharmaceutical Univ. Jpn
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TASHIRO Shin-ichi
Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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ONODERA Satoshi
Department of Clinical and Biomedical Sciences, Showa Pharmaceutical University
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IKEJIMA Takashi
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical Unive
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YU Jinghua
China-Japan Research Institute of Medical Pharmaceutical Sciences, Shenyang Pharmaceutical Universit
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LI Xiangru
China-Japan Research Institute of Medical Pharmaceutical Sciences, Shenyang Pharmaceutical Universit
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Yu Jinghua
China-japan Research Institute Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical Univer
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Li Xiangru
China-japan Research Institute Of Medical Pharmaceutical Sciences Shenyang Pharmaceutical University
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Onodera S
Dep. Of Clinical And Biomedical Sciences Showa Pharmaceutical Univ. Jpn
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Onodera Satoshi
昭和薬科大学 病態科
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Ikejima Takashi
China-japan Res. Inst. Of Medical And Pharmaceutical Sciences Shenyang Pharmaceutical Univ. Chn
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TASHIRO Shinichi
Department of Clinical and Biomedical Science, Showa Pharmeceutical University
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Tashiro Shin-ichi
Department Of Clinical And Biomedical Sciences Showa Pharmaceutical University
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Onodera Satoshi
Department Of Cinical And Biomedical Sciences Showa Pharmaceutical University
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Tashiro Shin-ichi
Department Of Cinical And Biomedical Sciences Showa Pharmaceutical University
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Tashiro S
Department Of Clinical And Biomedical Sciences Showa Pharmaceutical University
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Onodera S
Department Of Clinical And Biomedical Sciences Showa Pharmaceutical University
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Ikejima Takashi
China–Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University
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