| Project/Area Number |
16591287
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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 |
Digestive surgery
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| Research Institution | Akita University |
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Principal Investigator |
MIYAZAWA Hideaki Akita University, School of Medicine, Research Associate, 医学部, 助手 (10323148)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Tsutomu Akita University, School of Medicine, Associate Professor, 医学部, 助教授 (90235367)
IIDA Masatake Akita University, School of Medicine, Research Associate, 医学部, 助手 (90372325)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | liver epithelial cell / portal vein occlusion / splenic transposition / heat shock protein / heme oxygenase-1 / 肝虚血耐性 / 虚血再灌流傷害 / AFP陽性 / 肝幹細胞 / 低酸素耐性 / ヘムオキシゲナーゼ |
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| Research Abstract |
【Introduction】 A stem cell is known to have tolerance against hypoxic condition. We herein report that augmentation of hepatic stem cell (HSC) can induce tolerance against ischemia-reperfusion injury to the liver. 【IMethods】 (1) The portal trunk of S-D rat was ligated 3 weeks after splenic transposition and augmentation of HSC was verified. Then, rats were subjected to total liver ischemia of 60 minutes; 5 rats with PVO 3 days before ischemia (PVO group) and 5 rats without PVO (control group). (2) The role of heat shock protein (HSP) 72 and heme oxygenase (HO)-1 in the induction of the ischemic tolerance was investigated using Western blotting and immunohistochemistry.
【IResults】 (1) Serum AST and Alt levels 3 hours after reperfusion in the control group were 3,854±767IU/ and 5,345±1,722IU/L、while those in the PVO group were 1,813±169IU/ and 1,149±459IU/L, respectively(P<0.01). Histological examination 3 hours after reperfusion in the control group revealed massive coagulation necrosis, whereas hepatic architecture and the viability of hepatocytes were well preserved in the PVO group. (2) HSP72 was hardly detected in the liver after PVO. On the other hand, HO-1 was detected in the liver tissue by Western blotting and immunohistochemistry revealed the presence of HO-1 not in liver parenchymal cells but in many of sinusoidal lining cells.
【IConclusion】 The tolerance against ischemia-reperfusion injury was shown in rat liver 3 days after portal vein occlusion and augmentation of HSC might play a causative role in this tolerance. Induction of HSC can be a new strategy against ischemia-reperfusion injury. Stress proteins seemed not to play an important role in this ischemic tolerance, whole HO-1 appearing in the sinusoidal lining cells might relieve the liver damage.
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