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Chen G.,Cardiovascular Institute of Panyu District | Chen J.,Guangzhou University | Liu Q.,Guangzhou University | Ou C.,Southern Medical University | Gao J.,Nankai University
RSC Advances | Year: 2015

We report the phosphatase-triggered formation of a meta-stable peptide-based supramolecular hydrogel that can easily change to a clear solution by mechanical forces. Cells cultured in the hydrogel can therefore be separated by pipetting followed by centrifugation. © 2015 The Royal Society of Chemistry. Source

Zhang Z.,Cardiovascular Institute of Panyu District | Yan G.,Red Cross | Zhang W.,Cardiovascular Institute of Panyu District | Li J.,Cardiovascular Institute of Panyu District | And 5 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

To investigate the effect of atorvastatin on myocardial cell apoptosis, ventricular remodeling and cardiac function after acute myocardial infarction (AMI) in diabetic rats, and to explore whether the effect is mediated by hepatocyte growth factor (HGF)/c-Met signaling pathway. Diabetes in 70 male Sprague-Dawley rats was induced by intraperitoneal injection of streptozotocin (65 mg/kg). After 8 weeks, AMI was induced by the ligation of the left anterior descending coronary artery in the diabetic rats, and 32 surviving rats were randomly divided into AMI control group (n = 16) and atorvastatin intervention group (n = 16; 20 mg/kg/day). Similar surgical procedure was completed in sham group (n = 11) without coronary ligation. Atorvastatin was given daily by lavage from the first day after AMI. Two weeks later, the cardiac function, pathological changes of myocardial tissues, myocardial cell apoptosis, and the expression of HGF and c-Met were compared among groups using ultrasonography, hematoxylin and eosin staining and Masson staining, TUNEL assay, quantitative real-time polymerase chain reaction and immunohistochemical staining. AMI significantly reduced cardiac function, increased collagen volume fraction (CVF) and myocardial apoptotic index, and up-regulated the expression of HGF and c-Met at mRNA and protein levels in AMI control group (P < 0. 05). The cardiac function was improved, and CVF and myocardial apoptotic index were reduced by treatment with atorvastatin, which also up-regulated the expression of HGF and c-Met (P < 0. 05). The present study demonstrates that atorvastatin significantly attenuates myocardial apoptosis and cardiac remodeling, and improves cardiac function after AMI in diabetic rats by further enhancing the activation of HGF/c-Met pathway. © 2016, E-Century Publishing Corporation. All rights reserved. Source

Liang W.,Central Hospital of Panyu District | Liang W.,Cardiovascular Institute of Panyu District | Mo L.,Sun Yat Sen University | Ke X.,Sun Yat Sen University | And 8 more authors.
International Journal of Molecular Medicine | Year: 2016

Hyperglycemia, as well as diabetes mellitus, has been shown to impair ATP-sensitive K+ (KATP) channels in human vascular smooth muscle cells. Hydrogen sulfide (H2S) is also known to be an opener of KATP channels. We previously demonstrated the cardioprotective effects exerted by H2S against high-glucose (HG, 35 mM glucose)-induced injury in H9c2 cardiac cells. As such, we hypothesized that KATP channels play a role in the cardioprotective effects of H2S against HG-induced injury. In this study, to examine this hypothesis, H9c2 cardiac cells were treated with HG for 24 h to establish a model of HG-induced insults. Our findings revealed that treatment of the cells with HG markedly decreased the expression level of KATP channels. However, the decreased expression of KATP channels was reversed by the treatment of the cells with 400 M sodium hydrogen sulfide (NaHS, a donor of H2S) for 30 min prior to exposure to HG. Additionally, the HG-induced cardiomyocyte injuries, incluDing cytotoxicity, apoptosis, oxidative stress and mitochondrial damage, were ameliorated by treatment with NaHS or 100 M diazoxide (a mitochondrial KATP channel opener) or 50 M pinacidil (a non-selective KATP channel opener) for 30 min prior to exposure to HG, as indicated by an increase in cell viability, as well as a decrease in the number of apoptotic cells, the expression of cleaved caspase-3, the generation of reactive oxygen species (ROS) and the dissipation of mitochondrial membrane potential (MMP). Notably, treatment of the H9c2 cardiac cells with 100 M 5-hydroxydecanoic acid (5-HD, a mitochondrial KATP channel blocker) or 1 mM glibenclamide (Gli, a non-selective KATP channel blocker) for 30 min prior to treatment with NaHS and exposure to HG significantly attenuated the above-mentioned cardioprotective effects exerted by NaHS. Notably, treatment of the cells with 500 M N-acetylLcysteine (NAC, a scavenger of ROS) for 60 min prior to exposure to HG markedly reduced the HG-induced inhibitory effect on the expression of KATP channels. Taken together, our results suggest that KATP channels play an important role in the cardioprotective effects of exogenous H2S against HG-induced injury. This study also provides novel data demonstraring that there is an antagonistic interaction between ROS and KATP channels in HG-exposed H9c2 cardiac cells. Source

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