| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
Elevated serum free fatty acids and hepatocyte apoptosis are part of the features of nonalcoholic steatohepatitis (NASH). Cellular inhibitor of apoptosis (cIAP)-1 protein is an inhibitor of death receptor -mediated apoptosis. Aim of our study was to determine the role of cIAP-1 degradation during free fatty acid mediatedhepatocyte apoptosis.bcIAP-1 protein underwent degradation following treatment with palmitate in cultured HCC cells. SMAC mimetic JP1584, which induces rapid degradation of cIAP-1, significantly enhanced PA- mediated apoptosis in Mouse primary hepatocytes. However, JP 1584 did not sensitize primary hepatocytes from DR -/- mouse to apoptosis. These results indicated that degradation of cIAP-1 by PA enhances death receptor mediated pathway of lipoapoptosis. We are currently investigating the role of Troxerutin, a flavonoid, in FFA-mediated apoptosis. Troxerutin attenuated PA-mediated lipoapoptosis. We are currently investigating the mechanism that leads to this effect.
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