摘要
瞄准：在肝新生在四不同生长因素受体的表示的时间功课上调查试验性的部分肝切除术和 normothermic ischemia-reperfusion 损坏的效果。这由于在刺激肝新生的生长因素的潜在的治疗学的使用是相关的。方法：为部分肝切除术(PH ) ， 80% 肝质量是在 Sprague Dawley 老鼠的 resected。局部缺血和灌注(I/R ) 被门静脉和肝的动脉的吸藏为 15 min 导致。表皮的生长因素受体，肝的生长因素受体，成纤维细胞生长因素受体和瘤坏死因素 receptor-1 被免疫组织化学在损害以后分析直到 72 h。量的 RT-PCR 在最小的受体表示(24 h ) 的时间点被执行。结果：在免疫组织化学， EGFR， HGFR， FGFR 和 TNFR1 与一座山峰在部分肝切除术以后给双性人看了局面的动力学直到 12 h，在 24 h 以后的一个天底和另一弱增加直到 72 h。在肝新生期间，在局部缺血和灌注以后，受体表示更低；在在灌注以后的 24 h 的天底是一样。评估这个天底是否被 mRNA 抄写的缺乏引起，或由于一根柱子翻译规定， RT-PCR 在 24 h 并且与放松肝相比被执行。在每根探针，为受体有特定的 mRNA。EGFR， FGFR 和 TNFR1 mRNA 表示比在放松肝相等或低，在 I/R 以后的 HGFR 表示比在控制强壮。结论：部分至少由于 post-transcriptional 处理，在分析受体的表达式有一个天底在肝损伤以后的 24 h。因此，到在损坏以后的 stimulate 肝新生 24 h 的生长因素的治疗学的使用可能不是成功的。
AIM： To investigate the effects of experimental partial hepatectomy and normothermic ischemia-reperfusion damage on the time course of the expression of four different growth factor receptors in liver regeneration. This is relevant due to the potential therapeutic use of growth factors in stimulating liver regeneration. METHODS： For partial hepatectomy （PH） 80% of the liver mass was resected in Sprague Dawley rats. Ischemia and reperfusion （I/R） were induced by occlusion of the portal vein and the hepatic artery for 15 min. The epidermal growth factor receptor, hepatic growth factor receptor, fibroblast growth factor receptor and tumour necrosis factor receptor-1 were analysed by immunohistochemistry up to 72 h after injury. Quantitative RT-PCR was performed at the time point of minimal receptor expression （24 h）. RESULTS： In immunohistochemistry, EGFR, HGFR, FGFR and TNFR1 showed biphasic kinetics after partial hepatectomy with a peak up to 12 h, a nadir after 24 h and another weak increase up to 72 h. During liver regeneration, after ischemia and reperfusion, the receptor expression was lower; the nadir at 24 h after reperfusion was the same. To evaluate whether this nadir was caused by a lack of mRNA transcription, or due to a posttranslational regulation, RT-PCR was performed at 24 h and compared to resting liver. In every probe there was specific mRNA for the receptors. EGFR, FGFR and TNFR1 mRNA expression was equal or lower than in resting liver, HGFR expression after I/R was stronger than in the control. CONCLUSION： At least partially due to a post-transcriptional process, there is a nadir in the expression of the analysed receptors 24 h after liver injury. Therefore, a therapeutic use of growth factors to stimulate liverregeneration 24 h after the damage might be not successful.
