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Hou S.,Ningxia Medical University | Hou S.,Ningxia Key Laboratory of Cardiovascular and Cerebrovascular Diseases | Zheng F.,Ningxia Medical University | Li Y.,Ningxia Medical University | And 3 more authors.
International Journal of Molecular Sciences | Year: 2014

The aim of this study was to determine the beneficial effect of glycyrrhizic acid (GA) on type 2 diabetic nephropathy using renal tubular epithelial cell line (NRK-52E). The cells are divided into normal group (NG), high glucose group (HG), and treatment group (HG + GA). The methylthiazoletetrazolium (MTT) assay was used to detect the cell proliferation. Cell cycle analysis was performed using flow cytometry. Model driven architecture (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD) were also measured. Electron microscopy and histological were used to detect the changes in cell ultrastructure. The phosphorylation of AMP-activated protein kinase (AMPK), silent information regulator T1 (SIRT1), manganese-superoxide dismutase (Mn-SOD) and transforming growth factor-β1 (TGF-β1) were assessed by immunohistochemistry, immunofluorescence, and western blotting. Real-time fluorescent quantitative PCR (RT-qPCR) was used to measure Mn-SOD and PPARγ co-activator 1α (PGC-1a) mRNA. We find that high glucose increases NRK-52E cell proliferation and TGF-β1 expression, but decreases expression of AMPK, SIRT1 and Mn-SOD. These effects are significantly attenuated by GA. Our findings suggest that GA has protective effects against high glucose-induced cell proliferation and oxidative stress at least in part by increasing AMPK, SIRT1 and Mn-SOD expression in NRK-52E cells. © 2014 by the authors; licensee MDPI, Basel, Switzerland. Source


Yang A.-N.,Ningxia Medical University | Zhang H.-P.,Ningxia Key Laboratory of Cardiovascular and Cerebrovascular Diseases | Zhang H.-P.,Ningxia Medical University | Sun Y.,Ningxia Medical University | And 17 more authors.
FEBS Letters | Year: 2015

Homocysteine (Hcy) is an independent risk factor for atherosclerosis, but the underlying molecular mechanisms are not known. We investigated the effects of Hcy on fatty acid-binding protein 4 (FABP4), and tested our hypothesis that Hcy-induced atherosclerosis is mediated by increased FABP4 expression and decreased methylation. The FABP4 expression and DNA methylation was assessed in the aorta of ApoE-/- mice fed high-methionine diet for 20weeks. Over-expression of FABP4 enhanced accumulation of total cholesterol and cholesterol ester in foam cells. The up-regulation of DNA methyltransferase 1 (DNMT1) promoted the methylation process and decreased FABP4 expression. These data suggest that FABP4 plays a key role in Hcy-mediated disturbance of lipid metabolism and that DNMT1 may be a novel therapeutic target in Hcy-related atherosclerosis. © 2015 Federation of European Biochemical Societies. Source


Yang A.-N.,Ningxia Medical University | Zhang H.,Ningxia Medical University | Zhang H.-P.,Ningxia Key Laboratory of Cardiovascular and Cerebrovascular Diseases | Zhang H.-P.,Ningxia Medical University | And 17 more authors.
FEBS Letters | Year: 2015

Homocysteine (Hcy) is an independent risk factor for atherosclerosis, but the underlying molecular mechanisms are not known. We investigated the effects of Hcy on fatty acid-binding protein 4 (FABP4), and tested our hypothesis that Hcy-induced atherosclerosis is mediated by increased FABP4 expression and decreased methylation. The FABP4 expression and DNA methylation was assessed in the aorta of ApoE-/- mice fed high-methionine diet for 20 weeks. Over-expression of FABP4 enhanced accumulation of total cholesterol and cholesterol ester in foam cells. The up-regulation of DNA methyltransferase 1 (DNMT1) promoted the methylation process and decreased FABP4 expression. These data suggest that FABP4 plays a key role in Hcy-mediated disturbance of lipid metabolism and that DNMT1 may be a novel therapeutic target in Hcy-related atherosclerosis. © 2015 Federation of European Biochemical Societies. Source

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