Hepatic erythropoiesis is a characteristic event of the fetal liver. Generally, the erythropoiesis shows 4 phases: developing (embryonic day (ED) 10 to 14), maximum flat (ED 14 to 16), decreasing (ED 17 to 20), and disappearing day 1 to 10 after birth. In present study, TUNEL positive erythropoietic apoptotic cells were detected and increased through maximum flat phase, resulting in inducing decreasing phase. These results implicate that apoptosis is involved in the regulation of erythropoiesis in the fetal liver. Interestingly, the Bax over expressed in proerythroblasts and basophilic erythroblasts during developing phase, while Bcl-2 in polychromatic and acidophilic erythroblasts during decreasing phase. Moreover, in contrast to Bcl-2, Bax decreased from ED16, on which few erythropoietic cells were seen transiently. During disappearing phase, Bax increased by 2 to 3 times. But a rapid decline of Bcl-2 expression occurred on 1 day after birth. Thus, these results imply that the Bcl-2 and Bax play a role in proliferation and maturation of the erythropoietic cells by regulating apoptosis of the cells, in the hepatic erythropoiesis.
Animals ; Apoptosis ; Basophils ; Erythroblasts ; Erythropoiesis* ; In Situ Nick-End Labeling ; Liver ; Parturition ; Rats*

In this present study, we show that 3HK-induced reactive oxygen species (ROS) accumulation and caspase activation lead to apoptotic cell death. Pretreatment with N-acetylcysteine (NAC), an effective antioxidant, significantly attenuated 3HK-induced apoptosis by way of a reduction of ROS accumulation and caspase activity. SKN-SN cells were protected from 3HK-induced cytotoxicity by heat shock protein (HSP). HSP90 effectively attenuated 3HK-mediated ROS accumulation and apoptosis. In addition, the protective effect of HSP90 was abolished by pretreatment with HSP90 anti-sense oligonucleotide, but not when pretreated with anti-senses for other HSPs. These results suggest that HSP90 protects SKN-SH cells from 3HK-induced cytotoxicity by reducing ROS levels and caspase activity.
Acetylcysteine ; Apoptosis ; Cell Death* ; Heat-Shock Proteins* ; Hot Temperature* ; Reactive Oxygen Species*