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Authors = Jiayu Li

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Open AccessArticle Effects of the Activin A–Follistatin System on Myocardial Cell Apoptosis through the Endoplasmic Reticulum Stress Pathway in Heart Failure
Int. J. Mol. Sci. 2017, 18(2), 374; doi:10.3390/ijms18020374
Received: 23 November 2016 / Revised: 26 January 2017 / Accepted: 31 January 2017 / Published: 10 February 2017
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Abstract
Background: A previous study suggested that activin A inhibited myocardial cell apoptosis. This study thus aimed to explore the effects of the activin A–follistatin system on myocardial cell apoptosis in heart failure (HF) rats in order to determine whether or not the mechanism
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Background: A previous study suggested that activin A inhibited myocardial cell apoptosis. This study thus aimed to explore the effects of the activin A–follistatin system on myocardial cell apoptosis in heart failure (HF) rats in order to determine whether or not the mechanism operates through the endoplasmic reticulum stress (ERS) pathway. Methods: Myocardial infarction (MI) by vascular deprivation was used to induce HF. The enzyme-linked immunosorbent assay was used to detect activin A, follistatin and brain natriuretic peptide (BNP) contents in serum. Immunohistochemical staining for activin A, follistatin, CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP) and caspase-3 was performed on the myocardial tissue. The activin A-stimulated apoptosis of H9c2 cells was tested by flow cytometry. Western blot was used to detect the expression levels of activin A, follistatin and ERS-related proteins. Results: It was found that the high expression of activin A could cause activin A–follistatin system imbalance, inducing myocardial cell apoptosis via ERS in vivo. When HF developed to a certain stage, the expression of follistatin was upregulated to antagonize the expression of activin A. Activin A inhibited cardiomyocyte apoptosis with a low concentration and promoted apoptosis with a high concentration in vitro, also via ERS. Conclusion: Activin A–follistatin system participated in ERS-mediated myocardial cell apoptosis in HF. Full article
(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)
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Open AccessArticle Design, Synthesis and Antibacterial Evaluation of Some New 2-Phenyl-quinoline-4-carboxylic Acid Derivatives
Molecules 2016, 21(3), 340; doi:10.3390/molecules21030340
Received: 24 January 2016 / Revised: 19 February 2016 / Accepted: 7 March 2016 / Published: 10 March 2016
Cited by 3 | Viewed by 941 | PDF Full-text (464 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
A series of new 2-phenyl-quinoline-4-carboxylic acid derivatives was synthesized starting from aniline, 2-nitrobenzaldehyde, pyruvic acid followed by Doebner reaction, amidation, reduction, acylation and amination. All of the newly-synthesized compounds were characterized by 1H-NMR, 13C-NMR and HRMS. The antibacterial activities of these
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A series of new 2-phenyl-quinoline-4-carboxylic acid derivatives was synthesized starting from aniline, 2-nitrobenzaldehyde, pyruvic acid followed by Doebner reaction, amidation, reduction, acylation and amination. All of the newly-synthesized compounds were characterized by 1H-NMR, 13C-NMR and HRMS. The antibacterial activities of these compounds against Gram-negative (Escherichia coli, Pseudomonas aeruginosa) and Gram-positive bacteria (Staphylococcus aureus, Bacillus subtilis), as well as one strain of methicillin-resistant Staphylococcus aureus (MRSA) bacteria were evaluated by the agar diffusion method (zone of inhibition) and a broth dilution method (minimum inhibitory concentration (MIC)), and their structure-activity relationships were obtained and discussed. The results revealed that some compounds displayed good antibacterial activity against Staphylococcus aureus, and Compounds 5a4 and 5a7 showed the best inhibition with an MIC value of 64 μg/mL against Staphylococcus aureus and with an MIC value of 128 μg/mL against Escherichia coli, respectively. The results of the MTT assay illustrated the low cytotoxicity of Compound 5a4. Full article
(This article belongs to the Section Medicinal Chemistry)

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