Study on the improvement of liver injury by controlling sinusoidal cells and spleen

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1). Cold preservation and reperfusion injury of the liverApoptotic change in the liver was studied with Tunel method and electron microscopy in the cold preservation and reperfusion of the rat liver. Consequently, we found that apoptosis was occurred exclusively in the sinusoidal endothelial cells (SECs) with high incidence, leading to the detachment from the sinusoidal wall. This phenomenon was detected markedly in the cold preservation followed by reperfusion, but not in the cold preservation alone. Apoptosis in this experimental model was suppressed by vascular endothelial growth factor (VEGF) which has been well known to function as surviving and proliferative molecule. Furthermore, we showed that SEC of the fatty liver with cold storage was quite fragile and the size of the intra hepatocytic fatty droplet became larger in size as the cold preservation time was longer. These changes in the cold preserved fatty liver appeared to be one of the major causes of non-functioning graft which is frequently occurred in the fatty liver. We demonstrated that hepatocyte growth factor (HGF) ameliorated the impairment of SECs and inhibited enlargement of the fatty droplet. In addition, we showed that expressions of various kinds of the genes were changed during the cold preservation.2) Improvement of the liver cirrhosis by inhibition of activation of hepatic stellate cells. Previously, we reported that Y-27632, inhibitor of P160ROCK which is an effctor molecule of small G protein Rho, suppressed an activation of hepatic stellate cells, and that this compound inhibited the development into the liver cirrhosis in the CCL4-induced liver fibrosis of the rat. In the present study, we showed that Y-27632 ameliorated the already-established liver cirrhosis in the above-mentioned model without apparent side effects. This result may be a promising strategy for the liver cirrhosis.