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Background：Several studies have demonstrated that primary percutaneous coronary intervention （PCI） can result in reperfusion injury.This study aims to investigate the effectiveness of liposomal prostaglandin E l （Lipo-PGE1,Alprostadil,Beijing Tide Pharmaceutical Co.,Ltd.） for enhancing microcirculation in reperfusion injury.In addition,this study determined the optimal administration method for acute ST elevation myocardial infarction （STEMI） patients undergoing primary PCI.Methods：Totally,68 patients with STEMI were randomly assigned to two groups：intravenous administration ofLipo-PGE 1 （Group A）,and no Lipo-PGE1 administration （Group B）.The corrected thrombolysis in myocardial infarction （TIMI） frame count （cTFC） and myocardial blush grade （MBG） were calculated.Patients were followed up for 6 months.Major adverse cardiac events （MACE） were also measured.Results：There was no significant difference in the baseline characteristics between the two groups.The cTFC parameter in Group A was significantly lower than Group B （18.06 ± 2.06 vs.25.31 ± 2.59,P ＜ 0.01）.The ratio of final MBG grade-3 was significantly higher （P ＜ 0.05） in Group A （87.9％） relative to Group B （65.7％）.There was no significant difference between the two groups in final TIMI-3 flow and no-reflow.Patients were followed up for 6 months,and the occurrence of MACE in Group A was significantly lower than that in Group B （6.1％ vs.25.9％ respectively,P ＜ 0.05）.Conclusions：Myocardial microcirculation of reperfusion injury in patients with STEMI,after primary PCI,can be improved by administering Lipo-PGE1.

Aim： To examine the effects of a mixed formulation composed of prostaglandin E1 and lithium （PGEI＋Li mixture） on brain damage after cerebral ischemia. The effects of the mixture on protein expression of heat shock proteins （HSPs）, p53, and Bcl-2 were also determined. Methods： Brain ischemia was induced with a permanent middle cerebral artery occlusion （pMCAO） in rats. Rats were treated with a single intravenous administration of PGE1, lithium or a PGEI＋Li mixture immediately after the ischemic insult. The infarct volume and motor behavior deficits were analyzed 24 h after the ischemic insult. The protein levels of HSPTO, glucose-regulated protein 78 （GRP78）, HSP60, Bcl-2, and p53 in the striatum of the ipsilateral hemisphere were examined using immunoblotting. Results： The mixture （PGE1 22.6 nmol/kg＋Li 0.5 mmol/kg） reduced infarct volume and neurological deficits induced by focal cerebral ischemia. Moreover, the mixture had a greater neuroprotective effect against cerebral ischemia compared with PGE1 or lithium alone. The mixture was effective even if it was administered 3 h after ischemia. PGEI＋Li also significantly upregulated cytoprotective HSPTO GRP78, HSP60, and Bcl-2 protein levels, while decreasing p53 expression. Conclusion： These results demonstrated a PGEI＋Li mixture with a therapeutic window of up to 3 h for clinical treatment of cerebral ischemia. The PGEI＋Li mixture potentially exerts a protective effect after stroke through the induction of HSPs and Bcl-2 proteins.

Aim： To investigate the protective effects of prostaglandin E1 （PGE1） against H2O2-induced oxidative damage on human umbilical vein endothelial cells （HUVECs）. Methods： HUVECs were pretreated with PGE1 （0.25, 0.50, and 1.00 μmol/L） for 24 h and exposed to H2O2 （200 μmol/L） for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR. Results： PGE1 （0.25-1.00 μmol/L） was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H2O2. PGE1 also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE1 significantly increased NO content, eNOS protein, and mRNA expression. Conclusion： PGE1 effectively protected endothelial cells against oxidative stress induced by H2O2, an activity that might depend on the up-regulation of NO expression.