國立臺灣大學醫學院外科賴逸儒2006-07-262018-07-112006-07-262018-07-112003-07-31http://ntur.lib.ntu.edu.tw//handle/246246/24511Background: Hypoxic preconditioning (HP) confers cytoprotection against ischemia/reperfusion （I/R）injury, this effect is in part due to the induction of heme oxygenase-1. This experiment evaluates liver cell damage after I/R injury in HP rats. Methods： HP rats were prepared by exposure (15hours day-1) to an altitude chamber (5500m) for 2 weeks. Partial hepatic ischemia was produced in the left lobes for 45 minutes followed by 180 minutes of reperfusion. Zinc-protoporphyrin IX(ZnPP), a specific inhibitor of HO enzymatic activity, was subcutaneously injected 1 hour before the I/R injury in separate groups of sea-level （SL）control and HP rat. Serum alanine transaminase (ALT) levels, liver HO-1 mRNA and protein, and HO enzymatic activity were measured. Results：Heme oxygenase-1 (HO-1) was induced in the livers of rats exposed to HP. The levels of HO-1 mRNA and protein were obviously overexpressed after two weeks of hypoxic preconditioning. HP diminished the elevation of serum ALT levels after I/R injury （83.7±4.9 U L-1）when compared with SL controls （280.8±19.4 U L-1） and HP+ ZnPP pre-treated groups（151.3±4.4 U L-1）. The heme oxygenase activity in treated rats also correlated these results （237.9±19.8 pmol mg-1 protein hr-1 for the HP group, 164.3±12.7 pmol mg-1 protein hr-1 for the HP+ ZnPP, and 182.6±8.9 pmol mg-1 protein hr-1 for the SL controls. Conclusions：Our results indicated that the induction of HO-1 in hypoxic preconditioning played a protective role against hepatic I/R injury.application/pdf273124 bytesapplication/pdfzh-TW國立臺灣大學醫學院外科reporthttp://ntur.lib.ntu.edu.tw/bitstream/246246/24511/1/912314B002348.pdf