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Previous investigators have suggested that granulocyte colony-stimulating factor (G-CSF) may accelerate the healing process of liver lesions. This hypothesis has been discussed by some researchers. The action mechanisms remains unclear and further studies are needed to clarify this mechanism. To test this, we establish a rat model of liver injury using dimethylnitrosamine (DMN), transplanted the G-CSF into the rats. To determine whether G-CSF could prevent liver injury in DMN- intoxicated rats, we employed the model of acute and chronic liver injury induced by DMN: our study was limited to the characteristic changes in biochemical and histological parameters seen in liver damage. The DMN injections were given twice weekly for four weeks to establish liver damage. Rat was treated with DMN by intraperitoneal (IP) injection. On the 1st, 7th or 28th days, rats were sacrificed and liver histology was examined. Serial 5 µm sections of the liver were stained with hematoxylin and eosin (H&E). The serial measurement of the end products of hepatic synthetic activity also was used to assess liver damage. Liver injury was determined by biochemical and histological examination. As it is evident from results after administration of DMN, in addition to histologically changes of liver tissue, central vein, liver cord, sinusoids and bile duct were not normal, the activities of the serum liver enzymes also rose. Administration of G-CSF caused a statistically significantly decrease in the liver enzymes activity and sever of biochemical synthesis disruption in the liver. The protective role of G-CSF was showed in this rat model of acute and chronic liver damage induced by DMN. Our results showed beneficial effects of G-CSF treatment after liver injury on liver function. Histological and biochemical assessment of liver function revealed that liver tissue have a unique regenerative capability.       Key words: Dimethylnitrosamine, damage, granulocyte colony stimulating factor, liver.

Assessment effect of granulocyte colony-stimulating factor in experimental models of liver injury