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Gao M.,Capital Medical University | Gao M.,Beijing Institute of Heart Lung and Blood Vessel Diseases | Xie B.,Harbin Medical University | Gu C.,Capital Medical University | And 3 more authors.
Molecular Medicine Reports

Pulmonary dysfunction is one of the most frequent complications associated with cardiopulmonary bypass (CPB). Multiple factors, including the contact of blood with the artificial surface of the CPB circuit, ischemia-reperfusion and lung ventilator arrest elicit inflammatory reactions, consequently resulting in CPB-induced lung injury. The proinflammatory cytokine tumor necrosis factor-α (TNF-α) has been demonstrated to have a critical role in mediating CPB-induced pulmonary inflammation. The present review evaluated previous studies and summarized the effects of CPB on TNF-α level in the serum and lung tissue of patients and animal models of CPB, the underlying mechanism of TNF-α-mediated lung injury and the therapeutic strategies for the inhibition of TNF-α activity and production to attenuate CPB-induced lung injury. TNF-α level in the serum and lung tissue is significantly increased during and following CPB. TNF-α mediates CPB-induced lung damage by directly inducing apoptosis in alveolar epithelial cells and lung endothelial cells and by indirectly modulating the function of immune cells, including monocytes and macrophages. A functional neutralizing antibody to TNF-α can reduce pulmonary TNF-α production and attenuate CPB-induced lung injury in a rabbit model of CPB. Inhibition of TNF-α function and production using a neutralizing antibody to TNF-α appears to be a promising therapeutic strategy to alleviate CPB-induced lung injury. Source

Dai L.,Capital Medical University | Dai L.,Beijing Institute of Heart Lung and Blood Vessel Diseases | Gao M.,Capital Medical University | Gu C.,Capital Medical University | And 2 more authors.
European Journal of Cardio-thoracic Surgery

OBJECTIVES: Effective therapies to prevent vein graft failure after coronary artery bypass grafting (CABG) are still lacking. α-Cyanoacrylate (α-CA, 99% n-octyl-α-cyanoacrylate + n-butyl-α-cyanoacrylate) has been increasingly used as a tissue sealant for wound closure because of its bacteriostatic, biodegradable and haemostatic properties. As a strong tissue adhesive, α-CA might prevent an arterial circulation-induced mechanical stretch on vein graft to attenuate intimal hyperplasia. Here, we investigated the effects of perivenous application of α-CA on the vein graft in a rabbit model of carotid artery bypass grafting. METHODS: Healthy New Zealand white rabbits were randomized into no graft, graft or graft + α-CA group (n = 10 per group). Rabbit carotid artery was bypassed with the jugular vein. α-CA sealants were sprayed on the entire jugular graft including both anastomotic sites after completion of anastomoses. Blood flow parameters and histological characteristics of the vein grafts including vessel wall thickness, number of medial elastic lamina and proliferation index were evaluated 4 weeks after the surgery. The mRNA or protein levels of proinflammatory factors, chemokine (C-C motif) ligand-2 (CCL-2) and tumour necrosis factor-α (TNF-α) were measured 4 weeks after the operation by quantitative reverse transcription polymerase chain reaction or enzyme-linked immunosorbent assay. RESULTS: Compared with the untreated vein grafts at Week 4 after the operation, the α-CA spray significantly improved graft flow (39.4 ± 1.5 vs 27.8 ± 2.9 ml/min, P < 0.01), attenuated intimal and medial thickening (116.3 ± 1.0 vs 159.7 ± 0.9 μm, P < 0.01), reduced anti-proliferating cell nuclear antigen proliferation index of the vein grafts (15.0 ± 0.4 vs 23.6 ± 0.4%, P < 0.01), decreased the mRNA levels of plasminogen activator inhibitor-1 and CCL-2, and reduced the serum levels of TNF-α (92.9 ± 1.7 vs 102.7 ± 1.8 pg/ml, P < 0.01). CONCLUSION: Perivenous application of α-CA sealants exerts short-term beneficial effects on the vein graft and reduces inflammatory responses in a rabbit model of carotid artery bypass grafting. Long-term effects of α-CA on vein graft remodelling and the clinical significance of α-CA in CABG remain to be determined in future studies. © The Author 2015. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved. Source

Li J.-J.,Chinese Institute of Basic Medical Sciences | Zhang T.-P.,Chinese Institute of Basic Medical Sciences | Meng Y.,Capital Medical University | Du J.,Beijing Institute of Heart Lung and Blood Vessel Diseases | Li H.-H.,Capital Medical University
Cellular Physiology and Biochemistry

Backgroud: Atrogin-1/MAFbx is a major atrophy-related E3 ubiquitin ligase that functions as a negative regulator of cardiac hypertrophy. The mRNA expression of atrogin-1 is induced by oxidative stress via p38 mitogen-activated protein kinase (p38 MAPK). However, the molecular mechanisms that regulate the stability of atrogin-1 protein remain unclear. Methods: 293T and cardiac H9c2 cells were transfected with plasmids as indicated. The in vivo and in vitro ubiquitination assay and pulse-chase analysis were performed to detect the ubiquitination and stability of atrogin-1. The protein levels were measured by Western blot analysis. Results: We found that atrogin-1 underwent ubiquitin-mediated degradation by proteasome. The F-box motif of atrogin-1 and Skp1-Cul1-Roc1-F-box (SCF) complex are required for ubiquitination and degradation of atrogin-1. Furthermore, p38 MAPK signaling plays critical roles in regulating the ubiquitination and degradation of atrogin-1 as well as serum starvation-induced expression of atrogin-1 and reduction of H9c2 cell size. Conclusion: These findings may define a new mechanism for regulating the stability of atrogin-1 partially by p38 MAPK signaling. © 2011 S. Karger AG, Basel. Source

Wu W.-F.,Beijing Institute of Heart Lung and Blood Vessel Diseases | Wu W.-F.,Capital Medical University | Wang Q.-H.,Beijing Center for Physical and Chemical Analysis | Zhang T.,Capital Medical University | And 4 more authors.
Clinical Biochemistry

Objectives: We investigated the changes in cholesterol absorption and synthesis markers before and after simvastatin therapy in Chinese patients with coronary heart disease. Design and method: We developed a gas chromatography method to identify cholesterol synthesis and absorption markers and measured them in patients with coronary heart disease. We then tested their use in predicting the efficacy of simvastatin in lowering cholesterol. Serum samples from 45 patients and 38 healthy humans (controls) were analyzed in a gas chromatography-flame ionization detector. Results: Squalene and five non-cholesterol sterols-desmosterol and lathosterol (synthesis markers) and campesterol, stigmasterol, and sitosterol (absorption markers)-were detected. The recovery rates of the markers were 95-102%. After simvastatin treatment for four weeks, the total cholesterol and low-density lipoprotein cholesterol levels had significantly decreased from the baseline values (p<. 0.05). The baseline lathosterol level was significantly higher in good responders than in poor responders (p<. 0.05), and the stigmasterol level was significantly lower in good responders than in poor responders (p<. 0.05). Conclusions: This method should be suitable for the detection of serum squalene and non-cholesterol markers and can be used to predict the efficacy of simvastatin in patients with coronary heart disease. © 2013 The Canadian Society of Clinical Chemists. Source

Yong Q.,Capital Medical University | Guo R.,Capital Medical University | Chen Z.,Beijing Haidian Hospital | Li Z.,Capital Medical University | And 10 more authors.
Journal of Ultrasound in Medicine

Objectives: The purpose of this study was to evaluate the elasticity of the abdominal aorta in passively smoking rabbits using echo-tracking technology and pathologic examination.Methods: Fifty-four male New Zealand White rabbits were randomly divided into a passive smoking group and a normal control group. The elasticity indicators for the abdominal aorta of the rabbits were measured by means of echo tracking, which was performed before and 1, 2, and 3 months after passive smoking. Measured indicators included the pressure-strain elastic modulus, stiffness, arterial compliance, augmentation index, and pulse wave velocity. After the completion of the in vivo measurements, rabbits were euthanized randomly, and the corresponding arterial sites were resected for pathologic examination and in vitro measurement of vascular elasticity.Results: The echo-tracking technology used in our research proved that the elastic modulus, stiffness, and pulse wave velocity gradually increased with time by passive smoking, whereas arterial compliance decreased by passive smoking. Pathologic examination and in vitro measurements were performed and further confirmed the observed in vivo results.Conclusions: Passive smoking can injure arteries and reduce arterial elasticity. Echotracking technology is an accurate, noninvasive, and reliable method for analysis of the impact of passive smoking on arterial elasticity and detection arterial injury, which also can provide a new instructional basis for prevention and treatment of several arterial diseases. © 2014 by the American Institute of Ultrasound in Medicine. Source

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