AIM To investigate whether pretreatment with prostaglandin E 1 (PGE 1) might protect myocardium against peroxidative injury in early phase and in delayed phase. METHODS Rats were pretreated with PGE 1 (25 or 150 mg?kg -1 ). Isoproterenol (ISOP)(80 mg?kg -1 ) were injected peritoneally (ip) to induce acute myocardial infarction 20 minutes (early phase) or 24 hours (delayed phase) after pretreatment. Hearts were removed punctually 24 hours after ip ISOP and were assayed for content of malonaldehyde (MDA), activity of glutathione peroxidase (GSH Px) and superoxide dismutase (SOD). RESULTS ISOP caused myocardial injury with increased MDA content and SOD activity, and decreased GSH Px activity. Pretreatment with PGE 1, at each dose and in both phase, decreased the MDA content ( P

AIM To study the protective effects of prostaglandin E 1 on hypoxia/reoxygenation injury in cultured neonatal rat myocytes. METHODS The hypoxia/reoxygenation injury model of cultured neonatal rat myocardial cells was developed. The activities of plasma superoxide dismutase (SOD) were measured by the method of xanthine oxidase and the contents of serum malonicaldehyde (MDA) were determined by the method of thiobarbituric acid. The activities of dehydrogenase in mitochondria were detected by MTT assay. The activities of LDH in culture were also evaluated. CONCLUSION PGE 1 has protective effects on the cultured neonatal rat myocardial cells injured by hypoxia/reoxygenation. The mechanisms are related to its antioxidation effects.

AIMTo investigate the effects of prostaglandin E 1 on apoptosis induced by hypoxia/reoxygenation in cultured neonatal rat cardiomyocy tes. METHODSThe models of hypoxia/reoxygenation were made with t he first generation of cultured cardiomyocytes. Hypoxia/reoxygenation apoptosis in cultured neonatal rat cardiomyocytes was studied by agarose gel electrophores is and Tdt-mediated dUTP nick end labeling(TUNEL). Bcl-2 and bax mRNA were det ected by in situ hybridization. RESULTSThe results of DNA electr ophoresis in the H/R group showed the typical DNA ladder. And the DNA ladder decreased gradually corresponding to the increased dose of PGE 1. The TUNEL staining showed that the total number of apo ptotic cells in the H/R group was much biger than that in PGE 1(0 127 ?mol?L -1 ) group. The results of in situ hybridization showed that the conten t of bcl-2 mRNA in H/R group was lower than control. And the content of bax mRN A showed a reverse result as bcl-2 mRNA. Compared with H/R group, the content o f bcl-2 mRNA was significantly higher after treatment with PGE 1(0 014 ?mol ?L -1 , 0 042 ?mol?L -1 , 0 127 ?mol?L -1 ). But the content of bax mRNA in PGE 1(0 014 ?mol?L -1 , 0 042 ?mol?L -1 , 0 127 ?mol?L -1 )groups was significantly lower than H/R group. CONCLUSI ONH/R injury can induce cardiomyocyte apoptosis. PGE 1 has obvious an ti-apoptotic effects on cardiomyocyte and the mechanisms are possibly by inhibi ting the expression of bax and increasing the expression of bcl-2.hein creaseddoseofPGE1 .TheTUNELstainingshowedthatthetotalnumberofapoptoticcellsintheH