徳島大学 教育・研究者情報データベース(EDB)

1. (英) Sari Nurmila

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2. (英) Katanasaka Yasufumi

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3. (英) Sugiyama Yuga

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4. (英) Miyazaki Yusuke

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5. (英) Sunagawa Yoichi

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6. 船本 雅文([徳島大学.大学院医歯薬学研究部.医学域.先端医学教育研究プロジェクト]/[徳島大学.大学院医歯薬学研究部.医学域.医科学部門.生理系.薬理学])

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7. (英) Shimizu Kana

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8. (英) Shimizu Satoshi

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9. (英) Hasegawa Koji

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10. (英) Morimoto Tatsuya

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(英) Alpha Mangostin Derived from Garcinia magostana Linn Ameliorates Cardiomyocyte Hypertrophy and Fibroblast Phenotypes in Vitro.

(英) Cardiac hypertrophy and fibrosis are significant risk factors for chronic heart failure (HF). Since pharmacotherapy agents targeting these processes have not been established, we investigated the effect of alpha-magostin (α-man) on cardiomyocyte hypertrophy and fibrosis in vitro. Primary cultured cardiomyocytes and cardiac fibroblasts were prepared from neonatal rats. After α-man treatment, phenylephrine (PE) and transforming growth factor-beta (TGF-β) were added to the cardiomyocytes and cardiac fibroblasts to induce hypertrophic and fibrotic responses, respectively. Hypertrophic responses were assessed by measuring the cardiomyocyte surface area and hypertrophic gene expression levels. PE-induced phosphorylation of Akt, extracellular signal-regulated kinase (ERK)1/2, and p38 was examined by Western blotting. Fibrotic responses were assessed by measuring collagen synthesis, fibrotic gene expression levels, and myofibroblast differentiation. In addition, TGF-β-induced reactive oxygen species (ROS) production was investigated. In cultured cardiomyocytes, α-man significantly suppressed PE-induced increases in the cardiomyocyte surface area, and the mRNA levels (atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP)). Treatment with α-man significantly suppressed PE-induced Akt phosphorylation, but not ERK and p38 phosphorylation. In cultured cardiac fibroblasts, α-man significantly suppressed TGF-β-induced increases in L-proline incorporation, mRNA levels (POSTN and alpha-smooth muscle actin (α-SMA)), and myofibroblast differentiation. Additionally, it significantly inhibited TGF-β-induced reduced nicotinamide adenine dinucleotide phosphate oxidase4 (NOX4) expression and ROS production in cardiac fibroblasts. Treatment with α-man significantly ameliorates hypertrophy by inhibiting Akt phosphorylation in cardiomyocytes and fibrosis by inhibiting NOX4-generating ROS in fibroblasts. These findings suggest that α-man is a possible natural product for the prevention of cardiac hypertrophy and fibrosis.

1. (英) Animals
2. (英) Cardiomegaly
3. (英) Cells, Cultured
4. (英) Disease Models, Animal
5. (英) Fibroblasts
6. (英) Fibrosis
7. (英) Garcinia
8. 心臓(heart)
9. (英) Humans
10. 心筋(myocardium)
11. (英) Myocytes, Cardiac
12. (英) NADPH Oxidase 4
13. (英) Primary Cell Culture
14. (英) Rats
15. 活性酸素種(reactive oxygen species)
16. (英) Xanthones

1. (英) PublicationType: Journal Article