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   <subfield code="a">10.1007/s10620-010-1401-4</subfield>
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   <subfield code="a">Beneficial Effects of Follistatin in Hepatic Ischemia-Reperfusion Injuries in Rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Mami Kanamoto, Mitsuo Shimada, Yuji Morine, Tomoharu Yoshizumi, Satoru Imura, Toru Ikegami, Hiroki Mori, Yusuke Arakawa]</subfield>
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   <subfield code="a">Background: Ischemia-reperfusion injury has been demonstrated in a variety of clinical settings. The morbidity associated with liver transplantation and major hepatic resections is partly a result of ischemia-reperfusion injury. Follistatin, an activin-binding protein, binds to activins and subsequently blocks their action. It was reported that blockade of the action of activin with administration of follistatin accelerates recovery from ischemia renal injury. This study was conducted to investigate the involvement of the activin-follistatin system in hepatic ischemia-reperfusion injury. Methods: Total hepatic ischemia for 30min was performed followed by reperfusion in a rat model. Rats were divided into two groups: a follistatin group and a control group. Follistatin (1μg/body), which is an activin-binding protein, was administered at the time of reperfusion. Results: Though 80% of animals survived in the follistatin group, four of five animals died in the control group within 3days after reperfusion (p&lt;0.05). AST was significantly lower at 3h after reperfusion in the follistatin group (p&lt;0.05). LDH was also lower at 6h after reperfusion in the follistatin group (p&lt;0.05). Follistatin inhibited the mRNA expression of the βA subunit of activin. Moreover, the expression of IL-6, which is an inflammatory cytokine, was suppressed at 6h after reperfusion in the follistatin group (p&lt;0.05). Conclusions: The present study demonstrated that treatment with follistatin reduced the expression of IL-6 and activin resulting in beneficial support for hepatic ischemia-reperfusion injuries.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2010</subfield>
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   <subfield code="a">Hepatic ischemia-reperfusion injury</subfield>
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   <subfield code="a">Follistatin</subfield>
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   <subfield code="a">Cytokine</subfield>
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   <subfield code="a">Kanamoto</subfield>
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   <subfield code="u">Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, 770-8503, Tokushima, Japan</subfield>
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   <subfield code="a">Shimada</subfield>
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   <subfield code="u">Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, 770-8503, Tokushima, Japan</subfield>
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   <subfield code="a">Morine</subfield>
   <subfield code="D">Yuji</subfield>
   <subfield code="u">Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, 770-8503, Tokushima, Japan</subfield>
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   <subfield code="a">Yoshizumi</subfield>
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   <subfield code="u">Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, 770-8503, Tokushima, Japan</subfield>
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   <subfield code="u">Department of Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15, Kuramoto, 770-8503, Tokushima, Japan</subfield>
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