2011 Fiscal Year Final Research Report
Investigation of the regression of advanced atherosclerosis through the regulation of cellular senescence-custom-made therapy to Japanese elderly-
| Project/Area Number |
21590762
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General internal medicine (including Psychosomatic medicine)
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| Research Institution | Nagoya University |
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Principal Investigator |
HAYASHI Toshio 名古屋大学, 医学部附属病院, 講師 (80303634)
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| Co-Investigator(Kenkyū-buntansha) |
UMEGAKI Hiroyuki 名古屋大学, 医学部附属病院, 助教 (40345898)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 抗老化 / 動脈硬化性疾患 / 遺伝子制御 / 一酸化窒素 / 内皮機能制御 |
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| Research Abstract |
Aging is associated with diabetes and dyslipidemia as atherosclerosis characterized by endothelial dysfunction and oxidative stress leading NO destruction. We introduce one example. High glucose especially causes stress-induced premature and replicative senescence. We examined the regulatory role of various products on NO bioavailability, endothelial senescence and its functions. Exposure of HUVECs to high glucose for increased SA-βgalactosidase activity, a senescence marker, and decreased telomerase activity, a replicative senescence marker. We found the anti-senescent effect of statin, estrogen and citrulline. eNOSsiRNA reduced those effects. Streptozotocin-induced diabetes showed more senescent cells in endothelium of aged rats compared with age-matched control and insulin, statin or estrogen-treated rats. The regulatory effects of various products on endothelial senescence might be important for elderly medicine.
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