| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Outline of Final Research Achievements |
High glucose treatment (30 mM) significantly increased N-acetyl-beta-glucosaminidase (NAG) release, tumor necrosis factor (TNF)alpha/angiotensin II concentrations in cell media and p22phox protein levels compared with those in regular glucose medium (5.6 mM). Candesartan, an angiotensin II type 1 receptor (AT1R) blocker, showed a significant reduction on high glucose-induced NAG release, TNFalpha concentrations and p22phox protein levels in human renal proximal tubular epithelial cells (HK2 cells). In addition, significant decreases of NAG release, TNFalpha concentrations and p22phox protein levels in HK2 cells were observed in high glucose-treated group with thalidomide. AT1R knockdown with siRNA markedly reversed high glucose, angiotensin II or TNFalpha-induced p22phox protein levels in HK2 cells. TNFalpha may be involved in high glucose-induced renal tubular damage in HK2 cells possibly via AT1 receptor signaling.
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