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Pterostilbene attenuates myocardial ischemia-reperfusion injury via the phosphatidylinositol 3'-kinase-protein kinase B signaling pathway.

The current study aimed to evaluate the cardioprotective effects of pterostilbene (PTB) on myocardial ischemia-reperfusion (I/R) injury in rats and identify its possible underlying mechanisms of action. A rat I/R model was established by ligating the left anterior descending coronary artery for 30 min and releasing the ligature to induce reperfusion for 120 min. Serum creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) levels were measured using CK-MB and LDH assay kits and myeloperoxidase (MPO) activity in the myocardium was evaluated using an MPO assay kit. Tumor necrosis factor-α, interleukin (IL)-6 and IL-8 levels were assayed using ELISA kits. Cardiomyocyte apoptosis was measured using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Levels of protein kinase B (Akt) and phosphorylated Akt (p-Akt) were measured using western blotting. The results demonstrated that treatment with PTB significantly reduced cardiomyocyte apoptosis, significantly increased Bcl-2 and p-Akt levels and decreased Bax expression in the hearts of rats subjected to I/R injury. However, the protective effects induced by PTB were attenuated by LY294002, which inhibits Akt activation. The results of the current study suggest that PTB treatment may reduce the I/R injury-induced apoptosis of cardiomyocytes, which is mediated by the phosphoinositide 3-kinase/Akt signaling pathway.

2581 related Products with: Pterostilbene attenuates myocardial ischemia-reperfusion injury via the phosphatidylinositol 3'-kinase-protein kinase B signaling pathway.

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Diagnostic and clinical significance of the titin fragment in urine of Duchenne muscular dystrophy patients.

Duchenne muscular dystrophy (DMD) is a fatal progressive muscle wasting disease of childhood. Titin in sarcomere is digested by calcium dependent protease. To explore muscle damage in DMD, the urinary concentrations of the N-terminal fragment of titin were determined using a newly developed enzyme linked immune sorbent assay kit. The urinary titin concentrations were normalized to creatinine (Cr). A total of 145 urine samples were obtained at a single Japanese hospital from 113 DMD patients aged 3-29years. Normalized urinary titin concentration was 965.8±1011.9 (Mean±SD) pmol/mg Cr in patients with DMD. This was nearly 700-fold higher than healthy children (1.4±0.8pmol/mg Cr). The concentration was significantly higher in DMD than in BMD patients who had significantly higher urinary titin than normal. Urinary titin in DMD patients tended to decrease with age. The median concentration of urinary titin in the youngest (aged 3-7years) and oldest (aged ≥16years) groups was 1468.3 and 411.3pmol/mg Cr, respectively, with significant difference. Urinary concentration of titin correlated significantly with serum creatine kinase concentration, the best-known biomarker of DMD. The N-terminal fragment of titin in urine has potential as a diagnostic and clinical biomarker for DMD.

1596 related Products with: Diagnostic and clinical significance of the titin fragment in urine of Duchenne muscular dystrophy patients.

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[Grain-Moxibustion may Protect Myocardium by Reducing Oxidative Stress in Doxorubicin-induced Cardiomyopathy Rats].

To observe the effectiveness of grain-moxibustion in resisting oxidative stress in doxorubicin (DOX)-induced cardiomyopathy rats.

1424 related Products with: [Grain-Moxibustion may Protect Myocardium by Reducing Oxidative Stress in Doxorubicin-induced Cardiomyopathy Rats].

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Cardioprotective Effects of Malvidin Against Isoproterenol-Induced Myocardial Infarction in Rats: A Mechanistic Study.

BACKGROUND Malvidin (alvidin-3-glucoside) is a polyphenol that belongs to the class of natural anthocyanin, which is abundantly found in red wines, colored fruits, and the skin of red grapes. Therefore, the current investigation was intended to evaluate the effect of malvidin against myocardial infarction induced by isoproterenol in the rats. MATERIAL AND METHODS The cardioprotective effects was assessed by determining the effect of malvidin on the activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and on the levels of lipid peroxidation and serum marker enzymes. The serum levels of IL-6 and TNF-α were also determined using an enzyme-linked immunosorbent assay (ELISA) kit. RESULTS The present study demonstrated a significant cardioprotective effect of malvidin by restoring the defensive activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and by reducing the levels of lipid peroxidation and serum marker enzymes lactate dehydrogenase (LD) and creatine kinase (CK). Malvidin significantly ameliorated the histopathological changes and impaired mitochondria in the cardiac necrosis stimulated with isoproterenol. Additionally, the results also demonstrated that nuclear translocation of Nrf-2 and subsequent HO-1 expression might be associated with nuclear factor kappa B (NF-κB) pathway activation. CONCLUSIONS Our findings suggest that malvidin exerts cardioprotective effects that might be due to possible strong antioxidant and anti-inflammatory activities. Therefore, this study provides the basis for the development of malvidin as a safe and effective treatment of myocardial infarction.

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YiQiFuMai Powder Injection attenuates coronary artery ligation-induced myocardial remodeling and heart failure through modulating MAPKs signaling pathway.

YiQiFuMai Powder Injection (YQFM), a traditional Chinese medicine prescription re-developed based on Sheng-Mai-San, is a classical and traditional therapeutic for clinical heart failure (HF) and angina. However, its potential mechanism against HF remains unclear.

2948 related Products with: YiQiFuMai Powder Injection attenuates coronary artery ligation-induced myocardial remodeling and heart failure through modulating MAPKs signaling pathway.

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Apoptosis kinetics at reperfusion period in patients with acute ST-Segment Elevation Myocardial Infarction undergoing primary percutaneous coronary intervention and treated with thrombolytic therapy.

To evaluate the kinetics of cardiomyocyte apoptosis in patients undergoing primary percutaneous coronary intervention and thrombolytic therapy in order to elucidate the dark side of reperfusion injury.

2042 related Products with: Apoptosis kinetics at reperfusion period in patients with acute ST-Segment Elevation Myocardial Infarction undergoing primary percutaneous coronary intervention and treated with thrombolytic therapy.

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A reference interval study for common biochemical analytes in Eastern Turkey: a comparison of a reference population with laboratory data mining.

The aim of this study was to define the reference intervals (RIs) in a Turkish population living in Northeast Turkey (Erzurum) for 34 analytes using direct and indirect methods. In the present study, the regional RIs obtained were compared with other RI studies, primarily the nationwide study performed in Turkey.

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Cardioprotection provided by Echinatin against ischemia/reperfusion in isolated rat hearts.

This study evaluated the protective effect of Echinatin against myocardial ischemia/reperfusion (I/R) injury in rats.

2484 related Products with: Cardioprotection provided by Echinatin against ischemia/reperfusion in isolated rat hearts.

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Upregulated ATF6 contributes to chronic intermittent hypoxia-afforded protection against myocardial ischemia/reperfusion injury.

In the present study, we investigated the role of activating transcription factor 6 (ATF6) in the mechanism by which chronic intermittent hypoxia (CIH) increases tolerance to myocardial ischemia/reperfusion (I/R). Experiments were conducted using a rat model of I/R injury in vivo and isolated Langendorff-perfused rat hearts ex vivo. The role of Akt in this process was also investigated in vitro using rat myoblast H9c2 cells. Cell viability was measured using a cell counting kit-8 assay. Lactate dehydrogenase (LDH) and creatine kinase cardiac isoenzyme activity were also measured as markers of cellular damage. ATF6, Akt and phosphorylated (p)-Akt expression was analyzed by western blot analysis. RNA interference (RNAi) was used to suppress ATF6 expression. We noted that ATF6 expression in the ventricular myocardium was significantly increased in rats exposed to CIH. Furthermore, we noted that CIH preserved cardiac function after I/R in vivo and improved post-ischemic recovery of myocardial performance in isolated rat hearts. ATF6 and p-Akt expression was upregulated in cultured H9c2 cells exposed to chronic mild hypoxia compared with those cultured under normoxic conditions. Chronic mild hypoxia attenuated subsequent simulated I/R injury in H9c2 cells (48 h), as evidenced by increased cell viability and decreased LDH activity. By contrast, decreased cell viability and increased LDH activity were observed in siRNA-ATF6-transfected H9c2 cells, with a concomitant reduction in p-Akt levels. These results indicated that ATF6 upregulation is involved in the mechanism by which CIH attenuates myocardial I/R injury, possibly through upregulation of p-Akt, which is a key regulator of cardiomyocyte survival.

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Plasma concentration of high-mobility group box 1 (HMGB1) after 100 drop to vertical jumps and after a 1200-km bicycle race.

High-mobility group box 1 (HMGB1) has recently been reported to be involved in proinflammation and tissue repair. Therefore, we hypothesized that HMGB1 is released into the bloodstream after eccentric exercises or prolonged endurance activities. Blood samples from 11 participants that performed 100 drop to vertical jumps (DVJ) and from 10 participants that took part in the 1200-km 'Paris-Brest-Paris' bicycle race (PBP) were tested for HMGB1 and creatine kinase (CK) levels. CK increased after both DVJ (pre: 150.6 ± 81.5 U/L; post: 188.8 ± 95.5 U/L 8 h: 790.5 ± 346.4 U/L) and PBP (pre: 81.3 ± 36.4 U/L; post: 725.2 ± 229.5 U/L; 12 h: 535.8 ± 188.6 U/L), indicating membrane damage. However, HMGB1 plasma levels remained below the detection limit (78 pg/mL) of the applied enzyme-linked immunosorbent assay kit for all blood samples analysed. That is, neither high intensity eccentric exercises (DVJ) nor prolonged endurance events (PBP) seemed to affect HMGB1 levels in blood at selected time points.

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