.ALPHA.-Mangostin Induces Ca2+-ATPase-Dependent Apoptosis via Mitochondrial Pathway in PC12 Cells
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- Sato Ayumi
- Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University
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- Fujiwara Hironori
- Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University
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- Oku Hisae
- School of Pharmaceutical Sciences, Mukogawa Women’s University
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- Ishiguro Kyoko
- School of Pharmaceutical Sciences, Mukogawa Women’s University
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- Ohizumi Yasushi
- Department of Pharmaceutical Molecular Biology, Graduate School of Pharmaceutical Sciences, Tohoku University
Bibliographic Information
- Other Title
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- α-Mangostin Induces Ca〔2+〕-ATPase-Dependent Apoptosis via Mitochondrial Pathway in PC12 Cells
- アルファ Mangostin Induces Ca 2 ATPase Dependent Apoptosis via Mitochondrial Pathway in PC12 Cells
- α-Mangostin Induces Ca2+-ATPase-Dependent Apoptosis via Mitochondrial Pathway in PC12 Cells
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Abstract
We investigated the cell death effects of eight xanthones on PC12 rat pheochromocytoma cells. Among these compounds, α-mangostin, from the fruit hull of Garcinia mangostana L., had the most potent effect with the EC50 value of 4 μM. α-Mangostin-treated PC12 cells demonstrated typical apoptotic DNA fragmentation and caspase-3 cleavage (equivalent to activation). The flow cytometric analysis indicated that this compound induced apoptosis in time-and concentration-dependent manners. α-Mangostin showed the features of the mitochondrial apoptotic pathway such as mitochondrial membrane depolarization and cytochrome c release. Furthermore, α-mangostin inhibited the sarco(endo)plasmic reticulum Ca2+-ATPase markedly. There was a correlation between the Ca2+-ATPase inhibitory effects and the apoptotic effects of the xanthone derivatives. On the other hand, c-Jun NH2-terminal kinase (JNK/SAPK), one of the signaling molecules of endoplasmic reticulum (ER) stress, was activated with α-mangostin treatment. These results suggest that α-mangostin inhibits Ca2+-ATPase to cause apoptosis through the mitochondorial pathway.<br>
Journal
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 95 (1), 33-40, 2004
The Japanese Pharmacological Society
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Details 詳細情報について
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- CRID
- 1390001205175456512
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- NII Article ID
- 10013054384
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- NII Book ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL BIB ID
- 6944390
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- PubMed
- 15153648
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed