Pharmacologic preconditioning effects: Prostaglandin E 1 induces heat-shock proteins immediately after ischemia/reperfusion of the mouse liver

Prostaglandin E 1 (PGE 1 ) has several potential therapeutic effects, including cytoprotection, vasodilation, and inhibition of platelet aggregation. This study investigates the protective action of PGE 1 against hepatic ischemia/reperfusion injury in vivo using a complementary DNA microarray. PGE 1 or saline was continuously administered intravenously to mice in which the left lobe of the liver was made ischemic for 30 minutes and then reperfused. Livers were harvested 0, 10, and 30 minutes postreperfusion. Messenger RNA was extracted, and the samples were labeled with two different fluorescent dyes and hybridized to the RIKEN set of 18,816 full-length enriched mouse complementary DNA microarrays. Serum alanine aminotransferase and aspartate aminotransferase levels at 180 minutes postreperfusion were significantly lower in the PGE 1 -treated group than in the saline-treated group. The cDNA microarray analysis revealed that the genes encoding heat-shock protein (HSP) 70, glucose-regulated protein 78, HSP86, and glutathione S -transferase were upregulated at the end of the ischemic period (0 minutes postreperfusion) in the PGE 1 group. Our results suggested that PGE 1 induces HSPs immediately after ischemia reperfusion. HSPs might therefore play an important role in the protective effects of PGE 1 against ischemia/reperfusion injury of the liver.