Beneficial effects of follistatin in hepatic ischemia-reperfusion injuries in rats

Mami Kanamoto, Mitsuo Shimada, Yuji Morine, Tomoharu Yoshizumi, Satoru Imura, Toru Ikegami, Hiroki Mori, Yusuke Arakawa

Research output: Contribution to journalArticle

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Abstract

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 30 min was performed followed by reperfusion in a rat model. Rats were divided into two groups: a follistatin group and a control group. Follistatin (1 μg/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 3 days after reperfusion (p < 0.05). AST was significantly lower at 3 h after reperfusion in the follistatin group (p < 0.05). LDH was also lower at 6 h after reperfusion in the follistatin group (p < 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 6 h after reperfusion in the follistatin group (p < 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.

Original languageEnglish
Pages (from-to)1075-1081
Number of pages7
JournalDigestive Diseases and Sciences
Volume56
Issue number4
DOIs
Publication statusPublished - Apr 1 2011

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Follistatin
Reperfusion Injury
Liver
Activins
Reperfusion
Interleukin-6
Ischemia
Control Groups
Liver Transplantation

All Science Journal Classification (ASJC) codes

  • Physiology
  • Gastroenterology

Cite this

Beneficial effects of follistatin in hepatic ischemia-reperfusion injuries in rats. / Kanamoto, Mami; Shimada, Mitsuo; Morine, Yuji; Yoshizumi, Tomoharu; Imura, Satoru; Ikegami, Toru; Mori, Hiroki; Arakawa, Yusuke.

In: Digestive Diseases and Sciences, Vol. 56, No. 4, 01.04.2011, p. 1075-1081.

Research output: Contribution to journalArticle

Kanamoto, Mami ; Shimada, Mitsuo ; Morine, Yuji ; Yoshizumi, Tomoharu ; Imura, Satoru ; Ikegami, Toru ; Mori, Hiroki ; Arakawa, Yusuke. / Beneficial effects of follistatin in hepatic ischemia-reperfusion injuries in rats. In: Digestive Diseases and Sciences. 2011 ; Vol. 56, No. 4. pp. 1075-1081.
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AU - Kanamoto, Mami

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AU - Morine, Yuji

AU - Yoshizumi, Tomoharu

AU - Imura, Satoru

AU - Ikegami, Toru

AU - Mori, Hiroki

AU - Arakawa, Yusuke

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N2 - 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 30 min was performed followed by reperfusion in a rat model. Rats were divided into two groups: a follistatin group and a control group. Follistatin (1 μg/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 3 days after reperfusion (p < 0.05). AST was significantly lower at 3 h after reperfusion in the follistatin group (p < 0.05). LDH was also lower at 6 h after reperfusion in the follistatin group (p < 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 6 h after reperfusion in the follistatin group (p < 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.

AB - 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 30 min was performed followed by reperfusion in a rat model. Rats were divided into two groups: a follistatin group and a control group. Follistatin (1 μg/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 3 days after reperfusion (p < 0.05). AST was significantly lower at 3 h after reperfusion in the follistatin group (p < 0.05). LDH was also lower at 6 h after reperfusion in the follistatin group (p < 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 6 h after reperfusion in the follistatin group (p < 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.

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