Induction of Heat Shock Protein 72 by Heat Stress and its Protective Effect Against Ischemia-reperfusion Injury of the Rat Liver

Takamitsu Kasuya, Tsutomu Sato, Yasuhiko Sato, Tomoyuki Kusano, Yoshihiro Asanuma, Kenji Koyama

Department of Surgery, Akita University School of Medicine

To clarify the protective effect of induced heat shock protein (HSP) on hepatic ischemia-reperfusion injury, we determined the HSP 72 content and distribution after heat stress in normal and cirrhotic livers of rats by immunoblotting and immunostaining using anti-HSP 72 antibody, and then investigated DNA damage of the hepatocellular nuclei and measured the serum mitochondrial (m)-GOT value following inflow occlusion. The amount of HSP 72 was the highest 48 hours after the heat stress in both normal and cirrhotic livers, which was 3.9 times as high as in normal liver and 3.5 times as high in the cirrhotic liver as the pretreatment value. As for liver injury after inflow occlusion for 60 min in normal livers, there were no statistical differences in DNA damage and m-GOT values between the control and the HSP 72-induced group at the end of inflow occlusion. However, one hour after reperfusion, those damages were significantly lower in the HSP 72-induced group than in the control. On the other hand, in cirrhotic livers, there were no significant differences between the control and the HSP 72-induced group either at the end of ischemia or one hour after reperfusion. Consequently, it was concluded that a hepatic ischemiareperfusion injury can be reduced by the preinduction of HSP 72 in normal livers but not in cirrhotic livers.

Key words
heat shock protein, ischemia-reperfusion injury, DNA damage

Reprint requests
Takamitsu Kasuya Department of Surgery, Akita University School of Medicine
1-1-1 Hondo, Akita, 010-8543 JAPAN

Accepted
September 16, 1998

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