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1.
JAMA Intern Med ; 184(1): 100-101, 2024 Jan 01.
Article En | MEDLINE | ID: mdl-37983057

This case report describes a patient in their early 50s who presented with epigastric pain and jaundice and had significantly decreased heart rate after admission.


Myocardial Infarction , Humans , Electrocardiography , Arrhythmias, Cardiac
2.
BMC Pulm Med ; 22(1): 142, 2022 Apr 12.
Article En | MEDLINE | ID: mdl-35413880

BACKGROUND: Dapagliflozin, a selective inhibitor of sodium-glucose cotransporter 2 (SGLT2), can reduce cardiovascular events and mortality in patients with heart failure. A number of mechanisms have been proposed to explain the beneficial effects of SGLT2 inhibitors. The purpose of this study was to determine whether dapagliflozin can improve pulmonary vascular remodelling and the efficacy of dapagliflozin as an add-on therapy to sildenafil in rats with pulmonary arterial hypertension (PAH). METHODS: A monocrotaline (MCT)-induced PAH rat model was used in our study. MCT-injected rats were randomly divided into four groups and treated for 3 weeks with daily per os treatment with vehicle, dapagliflozin (1 mg/kg/day), sildenafil (25 mg/kg/day), or a combination of dapagliflozin (1 mg/kg/day) and sildenafil (25 mg/kg/day). Haemodynamic measurements, histological analysis, enzyme-linked immunosorbent assay and western blotting analysis were employed to detect the changes in PAH rats after treatments. RESULTS: Dapagliflozin significantly attenuated MCT-induced increases in right ventricular systolic pressure (RVSP) and right ventricular hypertrophy (RVH) in PAH rats. Dapagliflozin effectively decreased the thickening of pulmonary artery media and decreased the muscularization of pulmonary arterioles in PAH rats. Moreover, dapagliflozin attenuated nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation in lung tissues and the levels of interleukin-1ß (IL-1ß) and interleukin-18 (IL-18) in plasma. However, dapagliflozin as an add-on therapy to sildenafil in rats with PAH did not show a more pronounced beneficial effect on right ventricular systolic pressure and pulmonary vascular remodelling in MCT rats than sildenafil alone. CONCLUSIONS: Dapagliflozin reduces right ventricular systolic pressure and pulmonary vascular remodelling in a rat model of PAH. However, combination therapy with dapagliflozin and sildenafil was not more effective than monotherapy with sildenafil in PAH rats.


Hypertension, Pulmonary , Pulmonary Arterial Hypertension , Animals , Benzhydryl Compounds , Disease Models, Animal , Familial Primary Pulmonary Hypertension/metabolism , Glucosides , Humans , Hypertension, Pulmonary/chemically induced , Hypertension, Pulmonary/drug therapy , Hypertension, Pulmonary/metabolism , Monocrotaline , Pulmonary Arterial Hypertension/chemically induced , Pulmonary Arterial Hypertension/drug therapy , Pulmonary Artery , Rats , Sildenafil Citrate/pharmacology , Vascular Remodeling
3.
Acta Biochim Biophys Sin (Shanghai) ; 53(4): 430-437, 2021 Mar 26.
Article En | MEDLINE | ID: mdl-33686403

Resveratrol (RES) protects myocardial cells from hypoxia/reoxygenation (H/R)-caused injury. However, the mechanism of this effect has not been clarified. Thus, in this study, we aimed to determine whether RES attenuates H/R-induced cell necroptosis by inhibiting the tumor necrosis factor-alpha (TNF-α)/receptor-interacting protein kinase 1 (RIP1)/RIP3/mixed-lineage kinase domain-like (MLKL) signaling pathway. Rat myocardial ischemia/reperfusion (I/R) models and H/R-injured cell models were constructed. Our study showed that myocardial H/R injury significantly increased the levels of TNF-α, RIP1, RIP3, and p-MLKL/MLKL by western blot analysis. Cell viability assay and 4,6-dianmidino-2-phenylindole (DAPI)-propidium iodide staining showed that the cell viability was decreased, and necroptosis was increased after myocardial H/R injury. The expressions of TNF-α, RIP1, RIP3, and p-MLKL/MLKL in H/R myocardial cells treated with different concentrations of RES were significantly downregulated. In addition, we also found that the cell viability was increased and necroptosis was decreased in dose-dependent manners when H/R-injured cells were treated with RES. In addition, the enhanced effect of TNF-α on necroptosis in myocardial H/R-injured cells was improved by RES, and the effect of RES was confirmed in vivo in I/R rats. This study also showed that RES suppresses necroptosis in H9c2 cells, which may occur through the inhibition of the TNF-α/RIP1/RIP3/MLKL signaling pathway. Our data suggest that necroptosis is a promising therapeutic target and may be a promising therapeutic target for the treatment of myocardial I/R injury.


Myocardial Reperfusion Injury/metabolism , Necroptosis/drug effects , Protein Kinases/metabolism , Protein Serine-Threonine Kinases/metabolism , Receptor-Interacting Protein Serine-Threonine Kinases/metabolism , Resveratrol/pharmacology , Signal Transduction/drug effects , Tumor Necrosis Factor-alpha/metabolism , Animals , Male , Myocardial Reperfusion Injury/drug therapy , Myocardial Reperfusion Injury/pathology , Rats , Rats, Sprague-Dawley
5.
Biosci Rep ; 39(12)2019 12 20.
Article En | MEDLINE | ID: mdl-31782491

BACKGROUND: Prostaglandin-E1 (PGE1) is a potent vasodilator with anti-inflammatory and antiplatelet effects. However, the mechanism by which PGE1 contributes to the amelioration of cardiac injury remains unclear. METHODS: The present study was designed to investigate how PGE1 protects against hypoxia/reoxygenation (H/R)-induced injuries by regulating microRNA-21-5p (miR-21-5p) and fas ligand (FASLG). Rat H9C2 cells and isolated primary cardiomyocytes were cultured under hypoxic conditions for 6 h (6H, hypoxia for 6 h), and reoxygenated for periods of 6 (6R, reoxygenation for 6 h), 12, and 24 h, respectively. Cells from the 6H/6R group were treated with various doses of PGE1; after which, their levels of viability and apoptosis were detected. RESULTS: The 6H/6R treatment regimen induced the maximum level of H9C2 cell apoptosis, which was accompanied by the highest levels of Bcl-2-associated X protein (Bax) and cleaved-caspase-3 expression and the lowest level of B-cell lymphoma 2 (Bcl-2) expression. Treatment with PGE1 significantly diminished the cell cytotoxicity and apoptosis induced by the 6H/6R regimen, and also decreased expression of IL-2, IL-6, P-p65, TNF-α, and cleaved-caspase-3. In addition, we proved that PGE1 up-regulated miR-21-5p expression in rat cardiomyocytes exposed to conditions that produce H/R injury. FASLG was a direct target of miR-21-5p, and PGE1 reduced the ability of H/R-injured rat cardiomyocytes to undergo apoptosis by affecting the miR-21-5p/FASLG axis. In addition, we proved that PGE1 could protect primary cardiomyocytes against H/R-induced injuries. CONCLUSIONS: These results indicate that PGE1 exerts cardioprotective effects in H9C2 cells during H/R by regulating the miR-21-5p/FASLG axis.


Alprostadil/pharmacology , Fas Ligand Protein/genetics , MicroRNAs/genetics , Myocardial Reperfusion Injury/drug therapy , Reperfusion Injury/drug therapy , Animals , Apoptosis/drug effects , Cell Hypoxia/drug effects , Cell Hypoxia/genetics , Disease Models, Animal , Gene Expression Regulation/drug effects , Humans , Myocardial Reperfusion Injury/genetics , Myocardial Reperfusion Injury/pathology , Myocytes, Cardiac/metabolism , Myocytes, Cardiac/pathology , Protective Agents/pharmacology , Rats , Reperfusion Injury/genetics , Reperfusion Injury/pathology , Signal Transduction/drug effects
6.
Guang Pu Xue Yu Guang Pu Fen Xi ; 36(3): 806-10, 2016 Mar.
Article Zh | MEDLINE | ID: mdl-27400528

Total Volatile Basic Nitrogen (TVB-N) was usually taken as the physicochemical reference value to evaluate the mutton freshness. In order to explore the feasibility of hyperspectral (HSI) imaging technique to detect mutton freshness, 71 representative mutton samples were collected and scanned using a diffuse reflectance hyperspectral imaging (HSI) system in the Visible-Near infrared (NIR) spectral region (400-1 000 nm), and the chemical values of TVB-N content were determined using the semimicro Kjeldahl method according to the modified Chinese national standard. The representative spectra of mutton samples were extracted and obtained after selection of the region of interests (ROIs). The samples of calibration set and prediction set were divided at the ratio of 3 : 1 according to the content gradient method. Optimum HSI calibration models of the mutton (TVB-N) were established and evaluated by comparing different spectral preprocessing methods and modeling methods, which included Stepwise Multiple Linear Regression (SMLR), Partial Least Squares Regression (PLSR) and Principal Component Regression (PCR) methods. The results are that through the utilization of Multiplicative Scatter Correction (MSC), first derivative, Savitzky-Golay (S-G) smoothing and mean-centering together, both PLSR and PCR were able to achieve quantitative detection of mutton TVB-N. As for the PLSR model of mutton TVB-N established, the spectral pretreatment methods chosen included MSC, first derivative, S-G (15,2) smoothing and mean-centering, and the latent variables (LVs) number used was 11. As for the calibration set of PLSR model of mutton TVB-N, the correlation coefficient (r) and root mean square error of calibration (RMSEC) were 0.92 and 3.00 mg x (100 g)(-1), respectively. As for the prediction set of PLSR model of mutton TVB-N, the correlation coefficient (r), Root Mean Square Error of Prediction (RMSEP), and ratio of standard deviation to standard error of prediction (RPD) were 0.92, 3.46 mg x (100 g)(-1) and 2.35, respectively. The study demonstrated that the rapid and accurate analysis of TVB-N, the key freshness attribute, could be implemented by using the hyperspectral imaging (HSI) technique. The study provides the basis for further rapid and non-destructive detection of other mutton freshness attributes by using the hyperspectral imaging (HSI) technique, the improvement of current modeling effect of TVB-N content and the application involved of the technique in the practical production.


Meat/analysis , Nitrogen/analysis , Spectroscopy, Near-Infrared , Volatile Organic Compounds/analysis , Animals , Calibration , Food Quality , Least-Squares Analysis , Linear Models , Models, Theoretical , Sheep
7.
Zhongguo Zhong Yao Za Zhi ; 34(6): 740-3, 2009 Mar.
Article Zh | MEDLINE | ID: mdl-19624019

OBJECTIVE: To observe the effect of heart protection on diabetic cardiomyopathy in rats by tripterysium glucosides. METHOD: The rat diabetic cardiomyopathy rats model are made by streptozotocin, then divided into tripterysium glucosides group (n=8) and model group (n=8). In addition, the control group is established (n=8). Glucosides group was orally administrated tripterysium glucosides (18 mg x kg(-1)), the control groups was orally administrated same volume NS for 3 months. Blood sugar, heart function and cardiac index were detected after 3 months. Immunohistochemical techniques were used to detect NF-kappaB and ICAM-1 expression. Ultrastructure of cardiac muscle cell were observed by electronmicroscope. RESULT: Compared with model group, cardiac index was decreased after tripterysium glucosides administration, and LVSP, LVEDP, + dp/dtmax, -dp/dtmax, were improved, and the expression of nuclear Factor-kappaB (NF-kappaB) and intercellular adhension molecule-1 (ICAM-1) was inhibited. Ultrastructure of cardiac muscle cell such as mitochondrion and cardiac muscle fibers was atttenuated. CONCLUSION: Tripterysium glucosides could protect rat diabetic cardiomyopathy rats heart. These function may be related to inflammatory reaction inhibition and immunosuppression of tripterysium glucosides.


Cardiomyopathies/etiology , Diabetes Mellitus, Experimental/complications , Glucosides/pharmacology , Animals , Blood Glucose/metabolism , Cardiomyopathies/metabolism , Cardiomyopathies/pathology , Cardiomyopathies/physiopathology , Gene Expression Regulation/drug effects , Glucosides/administration & dosage , Glucosides/therapeutic use , Heart/drug effects , Intercellular Adhesion Molecule-1/metabolism , Male , Myocardium/ultrastructure , NF-kappa B/metabolism , Rats
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