Hepatic proliferation after partial liver irradiation in Sprague–Dawley rats

Abstract

The liver has powerful capability to proliferate in response to various injuries, but little is known as to liver proliferation after irradiation (IR) injury. This study investigated whether liver proliferation could be stimulated in low-dose irradiated liver by partial liver IR injury with high dose radiation. Sprague-Dawley rats were irradiated by 6-MV X-ray with single dose of 25Gy to the right-half liver, while the left-half liver was shielded (0.7Gy) or irradiated with single doses of 3.2, 5.6, and 8.0Gy, respectively. Hepatic proliferation in the shielded and low-dose irradiated left-half liver was evaluated by serum hepatic growth factor (HGF), proliferating cell nuclei antigen (PCNA), liver proliferation index (PI), hepatocyte mitosis index (MI). The observation time was 0day (before IR), 30, 60, 90, and 120days after IR. Our results showed that serum HGF and hepatocyte HGF mRNA increased after IR with HGF mRNA peak on day 30 in the shielded and low-dose irradiated left-half livers, and their values increased as the dose increased to the left-half liver. Liver PI and PCNA mRNA peaked on day 60 with stronger expressions in higher doses-irradiated livers. MI increased after IR, with the peak noted on day 60 in the shielded and on day 90 in the low-dose irradiated left-half livers. There was a 30day delay between MI peaks in the shielded and low-dose irradiated livers. In conclusion, 25Gy partial liver IR injury could stimulate the shielded liver and low-dose irradiated liver to proliferate. In the livers receiving a dose range of 3.2-8.0Gy, the proliferation was stronger in higher doses-irradiated liver than the low-dose irradiated. However, IR delayed hepatocyte mitosis.