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Background Hyperglycemia (HG) exacerbates myocardial ischemia/reperfusion (I/R) injury and renders protective strategies ineffective by amplified inflammatory response via enhanced high-mobility group box-1 (HMGB1) release. This study investigated the role of ethyl pyruvate (EP) against myocardial I/R injury under a clinically relevant HG condition. Methods Sprague-Dawley rats (n=76) were randomly assigned to 6 groups: normoglycemia (NG)-Sham, NG-I/R-control (C, saline), NG-I/R-EP treatment (50mg/kg) upon reperfusion, HG-Sham, HG-I/R-C, and HG-I/R-EP treatment upon reperfusion. HG was induced by 1.2g/kg dextrose. I/R was induced by ligation of the left anterior descending artery for 30min followed by 4h of reperfusion. Results HG resulted in exacerbation of myocardial infarct size by 19% with amplified activation of HMGB1–receptors of advanced glycation end products/toll like receptors–NF-κB pathway compared to NG following I/R, which all could be attenuated by EP. EP treatment was associated with diminished tumor necrosis factor-α, interleukin-1β, and interleukin-6 expressions. It also served to normalize the increase in pro-apoptotic Bax and the decrease in anti-apoptotic Bcl-2 protein levels. These effects were associated with decreased myocardial apoptosis and infarct size (by 30% and 36% in the NG and HG groups, respectively) regardless of the glycemic condition. Conclusion HG exacerbated myocardial I/R injury through amplified inflammatory response via increased HMGB1 level. EP treatment upon reperfusion conveyed significant myocardial protection against the I/R injury under both NG and HG conditions. Common to both glycemic conditions, associated mechanisms involved attenuated increase in HMGB1 level and suppression of its down-stream pathways.

Postharvest diseases cause considerable losses to harvested crops. Among them, gray mold (Botrytis cinerea) is a major problem of exporting to cut rose flowers into Korea. Irradiation treatment is an alternative to phytosanitary purposes and a useful nonchemical approach to the control of postharvest diseases. Gamma irradiation was evaluated for its in vitro and in vivo antifungal activity against B. cinerea on cut rose varieties, ‘Shooting Star’ and ‘Babe’. The irradiating dose required to reduce the population by 90%, D10, was 0.99kGy. Gamma irradiation showed complete inhibition of spore germination and mycelial growth of B. cinerea, especially 4.0kGy in vitro. Antifungal activity of gamma irradiation on rose B. cinerea is a dose-dependent manner. A significant phytotoxicity such as bent neck in cut rose quality was shown from gamma irradiation at over 0.4kGy (p

Erythropoietin (EPO), an essential hormone for erythropoiesis, provides protection against myocardial ischemia/reperfusion (I/R) injury. Hyperglycemia during acute myocardial infarction aggravates organ damage and attenuates the efficacies of various protective measures. This study aimed to investigate the protective role of EPO against myocardial I/R injury under a clinically relevant moderate hyperglycemic condition and its associated mechanisms. Eighty-two Sprague-Dawley rats were randomly assigned to six groups: normoglycemia-Sham, normoglycemia-I/R-control-saline (IRC), normoglycemia-I/R-EPO (IRE), hyperglycemia-Sham, hyperglycemia-IRC, and hyperglycemia-IRE. The rats received 1.2 g/kg dextrose or same volume of normal saline depending on the group. I/R was induced by a 30 min period of ischemia followed by reperfusion for 4 h. For 1 h before I/R injury, intravenous 4000 IU/kg of EPO was administered. EPO pretreatment significantly reduced the number of apoptotic cells and the infarct size compared with those of the control groups. EPO increased GATA-4 phosphorylation and acetylation against I/R in hyperglycemic myocardium. It also enhanced ERK induced GATA-4 post-translational modifications such as increased GATA-4 phosphorylation and acetylation, and decreased GATA-4 ubiquitination following hypoxia-reoxygenation in H9c2 cells in hyperglycemic medium. Increased GATA-4 stability by EPO diminished I/R-related down-regulation of Bcl-2 and reduction of caspase-3 activities in hyperglycemic myocardium. In conclusion, EPO pretreatment before I/R injury conveyed significant myocardial protection under moderate hyperglycemic condition through mechanisms involved in reduction of caspase-3 activity and up-regulation of Bcl-2 in association with enhanced ERK-induced GATA-4 stability.

InGaN layers with controlled In composition up to 30 at.% are grown on c-plane sapphire substrates by plasma-assisted molecular beam epitaxy. By considering the growth rate differences in GaN and InN caused by different vapor pressure and sticking coefficient, factors of the Ga and In source fluxes for the targeted In composition are determined. By applying the factors, InGaN layers with the almost same In compositions are grown. Before the growth the substrates were nitrided by rf-nitrogen plasma, which resulted in the formation of epitaxial AlN layer. The growth of thin GaN on this AlN surface shows strong streaky reflection high energy electron diffraction pattern with a specular spot, however, InGaN layers on the GaN layer show spotty patterns. Surface morphology of the InGaN layers shows island-like granules and the granule-like morphology is getting clear as the In composition and roughness are increased, too. The InGaN layers with In composition up to 30 at.% do not show formation of InN and only InGaN peaks are detected from the X-ray diffraction. Crystal quality of the InGaN layer with In composition of 15 at.% is worse than that of 30 at.%-In layer as addressed by larger broadening of X-ray rocking curves.

Dopaminergic neurons in the substantia nigra are particularly vulnerable, and their degeneration leads to Parkinson's disease. We have previously reported that matrix metalloproteinase-3 (MMP-3) activity is involved in dopaminergic neurodegeneration by multiple mechanisms and that this requires activation of MMP-3 from proMMP-3 by an intracellular serine protease. HtrA2/Omi is a mitochondrial serine protease that has been shown in non-dopaminergic cells to translocate into the cytosol where it triggers apoptosis. In the present study we sought to determine whether HtrA2/Omi might cause activation of MMP-3 in dopaminergic neuronal cells using CATH.a cell line. Mitochondrial stress induced by rotenone led to MMP-3 activation and HtrA2/Omi translocation into the cytosol. The MMP-3 activation involved HtrA2/Omi, because both pharmacological inhibition and siRNA-induced knockdown of HtrA2/Omi attenuated the activation induced by rotenone or MPP+. Overexpression of mature HtrA2/Omi, but not mutant HtrA2/Omi, resulted in MMP-3 activity increase and cell death. Addition of recombinant and catalytically active HtrA2/Omi to lysate of untreated cells led to activation of the endogenous MMP-3, and incubation of the HtrA2/Omi with recombinant proMMP-3 caused cleavage of proMMP-3 to a 48kD protein, corresponding to the active form, which was accompanied by an increase in MMP-3 activity. Taken together, the data indicate that HtrA2/Omi, which normally exists in the mitochondria, can cause MMP-3 activation in the cytosol under a cell stress condition, which can ultimately lead to demise of dopaminergic neuronal cells.

The present study was designed to investigate the anti-diabetic effect and mechanism of Korean red ginseng in C57BL/KsJ db/db mice. The db/db mice were divided into three groups: diabetic control group (DC), Korean red ginseng group (KRG, 100 ㎎/㎏) and metformin group (MET, 300 ㎎/㎏), and treated with drugs once per day for 10 weeks. Compared to the DC group, fasting blood glucose levels were decreased by 19.8% in KRG-, 67.7% in MET-treated group. With decreased plasma glucose and insulin levels, the insulin resistance index of the KRG-treated group was reduced by 27.6% compared to the DC group. The HbA1c levels in KRG and MET-treated groups were also decreased by 11.0% and 18.9% compared to that of DC group, respectively. Plasma triglyceride and non-esterified fatty acid levels were decreased by 18.8% and 16.8%, respectively, and plasma adiponectin and leptin levels were increased by 20.6% and 12.1%, respectively, in the KRG-treated group compared to those in DC group. Histological analyses of the liver and fat tissue of mice treated with KRG revealed significantly decreased number of lipid droplets and decreased size of adipocytes compared to the DC group. From the pancreatic islet double-immunofluorescence staining, we observed KRG has increased insulin contents, but decreased glucagon production. To elucidate action mechanism of KRG, effects on AMPactivated protein kinase (AMPK) and its downstream target proteins responsible for fatty acid oxidation and gluconeogenesis were explored in the liver. KRG activated AMPK and acetyl-coA carboxylase (ACC) phosphorylations, resulting in stimulation of fatty acid oxidation. KRG also caused to down regulation of SREBP1a and its target gene expressions such as FAS, SCD1 and GPAT. In summary, our results suggest that KRG exerted the anti-diabetic effect through AMPK activation in the liver of db/db mice.