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Antimutagenic Activity of Sakuranetin from Prunus Jamasakura (2003)

Miyazawa, M. ; Kinoshita, H. ; Okuno, Y.

Oxford, UK : Blackwell Publishing Ltd

Journal of food science 68 (2003), S. 0

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ISSN: 1750-3841

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology

Notes: : Sakuranetin (compound 1) from bark of Prunus jamasakura showed a suppressive effect on umu gene expression of SOS response in Salmonella typhimurium TA1535/pSK1002 against the mutagen furylfuramide. Gene expression was suppressed 83% at a concentration of 0.70 μmol/mL. The ID50 value of compound 1 was 0.30 μmol/mL. This compound showed the suppression of 4NQO, MNNG, Trp-P-1, AfB1, activated Trp-P-1, and UV irradiation-induced SOS response. The methylated derivative (compound 2) of compound 1 showed less suppressive effect against all mutagens than compound 1. The antimutagenic activities of compounds 1 and 2 against furylfuramide, Trp-P-1, and activated Trp-P-1 were assayed by the Ames test using the S. typhimurium TA100 strain.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1365-2621.2003.tb14113.x

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Mechanism of atherosclerotic calcification (2000)

Shioi, A. ; Mori, K. ; Jono, S. ; [et al.]

Springer

Zeitschrift für Kardiologie 89 (2000), S. S075

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ISSN: 1435-1285

Keywords: Key words Alkaline phosphatase – atherosclerosis – calciotropic hormones – 1α-hygroxylase – macrophages – osteoblastic differentiation – sodium-dependent phosphate cotransport – vascular smooth muscle cells

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary Calcification is almost invariably associated with atherosclerotic plaque lesions. Recent data suggest that plaque calcification is an active, regulated process similar to osteogenesis. In order to clarify the mechanism of plaque calcification, we developed an in vitro model of vascular calcification by utilizing bovine vascular smooth muscle cells (BVSMCs). This model is useful in that diffuse and massive calcification can be induced within 2 weeks and thereby biochemical analyses of vascular calcification can be performed. We have analyzed several aspects of vascular calcification by using this model and demonstrated as follows: 1) in vitro calcification of BVSMCs is regulated by calciotropic hormones and BVSMCs are equipped with a unique autocrine and/or paracrine system regulating calcium metabolism. 2) Sodium-dependent phosphate cotransport plays a crucial role in BVSMC calcification as well as in mineralization of skeletal tissues. 3) BVSMCs acquire osteoblastic phenotype under certain conditions. Finally, we discuss the roles of macrophages in the development of atherosclerotic calcification. Interferon-γ (INF-γ) induces gene expression of 25-hydrovitamin D-1α-hydroxylase (1αOhase) and its activity in macrophages. Since 1αOhase can locally convert 25-hydroxyvitamin D into 1α,25-dihydroxyvitamin D (1,25(OH)2D), an active metabolite of vitamin D, it is suggested that local production of 1,25(OH)2D by macrophages may promote atherosclerotic calcification. Moreover, macrophages may be involved in the phenotypic changes of vascular smooth muscle cells (VSMCs) to acquire calcifying capacity. Therefore, the phenotypic changes of VSMCs in atherosclerotic plaque may contribute to the development of atherosclerotic calcification.