| Project/Area Number |
18K15264
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 50020:Tumor diagnostics and therapeutics-related
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| Research Institution | Gunma University |
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Principal Investigator |
Ishii Norihiro 群馬大学, 医学部附属病院, 助教 (00711508)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 肝硬変 / 肝線維化 / Galectin-3 / 星細胞 / Kupffer細胞 / M2BPGi / 肝星細胞 / 線維化 |
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| Outline of Final Research Achievements |
From our study of M2BPGi in liver cirrhosis, co-activation between hepatic stellate cells and Kupffer cells is considered to be important for the progression of liver fibrosis. So we examined the effect of novel galectin-3 inhibitor. In the cell proliferation assay, novel galectin-3 inhibitor for hepatic stellate cells showed the suppressive effect in a dose dependent manner. Moreover, in the western blotting, novel galectin-3 inhibitor suppressed the expression of α-SMA which is a activation marker for stellate cells. Thus, novel galectin-3 inhibitor has a suppressive effect for the activation of hepatic stellate cells. On the other hand, this novel galectin-3 inhibitor has been confirmed to be effective also in the in vivo xenograft model with fibrosis, this new drug are expected to be applied for the liver fibrosis model in the future.
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| Academic Significance and Societal Importance of the Research Achievements |
肝硬変は慢性的な肝障害により肝細胞が線維組織で置換され、肝臓の硬化と肝機能の低下 をきたした状態であり、日本における患者数は約40万人とされている。また、肝硬変に伴う肝癌の発癌も重要な問題である。肝線維化に対する有効な治療薬は現時点ではまだなく、新規Galectin-3阻害剤は肝星細胞とKupffer細胞の連関を遮断し、肝の線維化を抑制する新たな治療戦略になりうると考えられる。
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