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Malignant glioma is the most common type of brain tumor with poor clinical outcome and survival. Therefore, it is imperative to develop novel therapeutic agents for managing glioma. The aim of this study was to investigate the role of amentoflavone (AF), an active flavonoid component in Selaginella tamariscina Spring, in glioma cells and the underlying mechanism of its action. Our results showed that miR-124-3p expression was significantly down-regulated in glioma tissues relative to normal brain tissues. AF decreased cell viability and triggered apoptosis in both glioma cell lines in a dose-dependent manner. AF induced apoptosis and inhibited glycolysis in the glioma cells by upregulating miR-124-3p. Furthermore, AF upregulated miR-124-3p by repressing DNMT1 through Sp1, which in turn was caused by the activation of ROS/AMPK signaling pathway by AF. In conclusion, AF could induce apoptosis and inhibited glycolysis in glioma cells via miR-124-3p. Our findings provide preliminary experimental data that support further investigation on the therapeutic efficacy of AF in glioma., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Podocytes are the major sites of vascular endothelial growth factor (VEGF) production in kidneys. Over-expression of VEGF is involved in the pathogenesis of diabetic nephropathy (DN), and an emerging body of evidence suggests that autophagy plays an important role in DN. In this study, the effect of autophagy on over-expressed VEGF along with its underlying mechanism was investigated in streptozotocin (STZ)-induced diabetic mice and high glucose (HG)-induced podocytes. We found that diabetes caused podocyte foot process effacement and VEGF upregulation significantly. In vitro, high glucose induced VEGF and reduced the podocyte viability. After treatment with rapamycin in podocytes, an autophagy inducer, VEGF activation was significantly abrogated and podocyte injury was ameliorated. In contrast, podocytes treated with 3-methyladenine (3-MA), a potent autophagy inhibitor, had increased VEGF expression. Furthermore, 3-MA significantly increased the production of HG-induced reactive oxygen species (ROS), whereas rapamycin decreased the cellular ROS level. Inhibition of ROS production by N-acetyl-l-cysteine (NAC) effectively reduced the over-expression of VEGF. These studies show the vital role of autophagy in the regulation of VEGF, which presents a protective effect on HG-induced podocyte injury. ROS production may be an important mechanism for mediating this process.

Background and Objectives: Low protein diets supplemented with keto acid (sLPD) are recommended for patients with stage 3-5 chronic kidney disease (CKD). This study assessed whether sLPD is beneficial for patients with steroid-resistant proteinuria during early-stage CKD., Design, Setting, Participants, and Measurements: A 1-year randomized controlled trial was conducted from 2010 to 2012. In this study, 108 proteinuric patients who were steroid-resistant were assigned to a sLPD group (0.6 g/kg/d with 0.09 g/kg/d keto acids) or a normal protein diet group (NPD, 1.0 g/kg/d). Estimated dietary protein intake, urinary protein excretion, remission rate, renal function, nutritional status, and blood pressure were measured., Results: Baseline characteristics were comparable between the sLPD group (47 patients) and the NPD group (49 patients). Urinary protein excretion significantly decreased in sLPD compared to NPD in months 6, 9, and 12 (P<0.05). Proteinuria reduction was higher in sLPD than in NPD (P<0.001) at the end of the study. Complete remission and partial remission rates were higher in sLPD than in NPD. Serum albumin and pre-albumin levels were higher in sLPD than in NPD in months 9 and 12 (P<0.05). Serum total cholesterol and triglyceride levels declined more significantly in sLPD than in NPD (P<0.01) at the end of the study. There were no differences in nutritional status, renal function, hemoglobin, or blood pressure between the two groups., Conclusions: sLPD is both nutritionally safe and beneficial, providing nephroprotective effects for early-stage CKD patients with steroid-resistant proteinuria.