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Total 44 results found since Jan 2013.

Simvastatin protects Sertoli cells against cisplatin cytotoxicity through enhanced gap junction intercellular communication.
Authors: Wang L, Peng J, Huang H, Wang Q, Yu M, Tao L Abstract Cisplatin, an important chemotherapeutic agent against testicular germ cell cancer, induces testicular toxicity on Leydig and Sertoli cells, leading to serious side-effects such as azoospermia and infertility. In a previous study, it was found that simvastatin enhanced the sensitivity of Leydig tumor cells to chemotherapeutic toxicity through the enhancement of gap junction functions. In the present study, the effect of simvastatin on the sensitivity of normal Sertoli cells to cisplatin and the role of gap junctions in such effects was investigated. T...
Source: Oncology Reports - August 15, 2015 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Abstract 16: Combination simvastatin and metformin induces G1-phase cell cycle arrest and Ripk1- and Ripk3-dependent necroptosis in C4-2B osseous metastatic castration-resistant prostate cancer cells
Castration-resistant prostate cancer (CRPC) cells acquire resistance to chemotherapy and apoptosis in part due to enhanced aerobic glycolysis and biomass production, known as Warburg effect. We previously demonstrated that combination simvastatin (SIM) and metformin (MET) ameliorates critical Warburg effect-related metabolic aberrations of C4-2B cells, synergistically and significantly decreases CRPC cell viability and metastatic properties, with minimal effect on normal prostate epithelial cells, and inhibits primary prostate tumor growth, metastasis, and biochemical failure in an orthotopic model of metastatic CRPC, more...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Babcook, M. A., Sramkoski, R. M., Fujioka, H., Daneshgari, F., Almasan, A., Shukla, S., Gupta, S. Tags: Molecular and Cellular Biology Source Type: research

Molecular Hydrogen stabilizes atherosclerotic plaque in low-density lipoprotein receptor knockout mice.
CONCLUSIONS: The inhibitory effects of H2 on the apoptosis of macrophage-derived foam cells, which take effect by suppressing the activation of ERS pathway and by activating Nrf2 antioxidant pathway, might lead to an improvement in atherosclerotic plaque stability. PMID: 26117323 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - June 24, 2015 Category: Biology Authors: Song G, Zong C, Zhang Z, Yu Y, Yao S, Jiao P, Tian H, Zhai L, Zhao H, Tian S, Zhang X, Wu Y, Sun X, Qin S Tags: Free Radic Biol Med Source Type: research

Drug Repurposing Screen Identifies Foxo1-Dependent Angiopoietin-2 Regulation in Sepsis*
Conclusions: 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors may operate through a novel Foxo1-angiopoietin-2 mechanism to suppress de novo production of angiopoietin-2 and thereby ameliorate manifestations of sepsis. Given angiopoietin-2’s dual role as a biomarker and candidate disease mediator, early serum angiopoietin-2 measurement may serve as a stratification tool for future trials of drugs targeting vascular leakage.
Source: Critical Care Medicine - June 17, 2015 Category: Emergency Medicine Tags: Online Laboratory Investigations Source Type: research

Autocrine secretion of 15d‐PGJ2 mediates simvastatin‐induced apoptotic burst in human metastatic melanoma cells
Conclusions and ImplicationsWe characterized simvastatin‐induced activation of the 15d‐PGJ2/FABP5 signalling cascades, which triggered an apoptotic burst in melanoma cells but did not affect primary human melanocytes. These data support the rationale for the pharmacological targeting of 15d‐PGJ2 in metastatic melanoma.
Source: British Journal of Pharmacology - December 1, 2014 Category: Drugs & Pharmacology Authors: Christine Wasinger, Martin Künzl, Christoph Minichsdorfer, Christoph Höller, Maria Zellner, Martin Hohenegger Tags: RESEARCH PAPER Source Type: research

Synergistic Effect of Sulindac and Simvastatin on Apoptosis in Lung Cancer A549 Cells through ...
Conclusion Combined treatment with sulindac and simvastatin augmented their apoptotic potential in lung cancer cells through AKT signaling-dependent downregulation of survivin. These results indicate that sulindac and simvastatin may be clinically promising therapies for the prevention of lung cancer.
Source: Cancer Research and Treatment - October 26, 2014 Category: Cancer & Oncology Tags: Original Article Source Type: research

Simvastatin induces NFκB/p65 down-regulation and JNK1/c-Jun/ATF-2 activation, leading to matrix metalloproteinase-9 (MMP-9) but not MMP-2 down-regulation in human leukemia cells.
Abstract The aim of the present study was to explore the signaling pathways associated with the effect of simvastatin on matrix metalloproteinase-2 (MMP-2)/MMP-9 expression in human leukemia K562 cells. In sharp contrast to its insignificant effect on MMP-2, simvastatin down-regulated MMP-9 protein expression and mRNA levels in K562 cells. Simvastatin-induced Pin1 down-regulation evoked NFκB/p65 degradation. Meanwhile, simvastatin induced JNK-mediated c-Jun and ATF-2 activation. Over-expression of Pin1 suppressed simvastatin-induced MMP-9 down-regulation. Treatment with SP600125 (a JNK inhibitor) or knock-down of...
Source: Biochemical Pharmacology - October 11, 2014 Category: Drugs & Pharmacology Authors: Chen YJ, Chang LS Tags: Biochem Pharmacol Source Type: research

Autocrine secretion of 15d‐PGJ2 mediates simvastatin induced apoptotic burst in human metastatic melanoma cells
ConclusionWe here delineate simvastatin induced activation of the 15d‐PGJ2/FABP5 signalling cascades, which trigger an apoptotic burst in melanoma cells, while primary human melanocytes were unaffected. These data support new rational ground for pharmacological targeting of 15d‐PGJ2 in metastatic melanoma.
Source: British Journal of Pharmacology - August 4, 2014 Category: Drugs & Pharmacology Authors: Christine Wasinger, Martin Künzl, Christoph Minichsdorfer, Christoph Höller, Maria Zellner, Martin Hohenegger Tags: Research Paper Source Type: research

Effect of simvastatin on the resistance to EGFR tyrosine kinase inhibitors in a non-small cell lung cancer with the T790M mutation of EGFR.
This study investigated overcoming resistance to EGFR-TKI using simvastatin. We demonstrated that addition of simvastatin to gefitinib enhanced caspase-dependent apoptosis in T790M mutant NSCLC cells. Simvastatin also strongly inhibited AKT activation, leading to suppression of β-catenin activity and the expression of its targets, survivin and cyclin D1. Both insulin treatment and AKT overexpression markedly increased p-β-catenin and survivin levels, even in the presence of gefitinib and simvastatin. However, inhibition of AKT by siRNA or LY294002 treatment decreased p-β-catenin and survivin levels. To determine the rol...
Source: Experimental Cell Research - March 12, 2014 Category: Cytology Authors: Hwang KE, Kwon SJ, Kim YS, Park DS, Kim BR, Yoon KH, Jeong ET, Kim HR Tags: Exp Cell Res Source Type: research

RhoA‐Mediated Inhibition of Vascular Endothelial Cell Mobility: Positive Feedback Through Reduced Cytosolic p21 and p27
In this study, we investigated the mechanisms of 3MC‐mediated downregulation of cytosolic p21/ p27, and the effects of 3MC on RhoA activation and cell migration, in mouse cerebral vascular endothelial cells (MCVECs). Our results indicated that 3MC reduced the phosphorylation of p21/p27 through AhR/RhoA/PTEN‐mediated PI3K/Akt inactivation, which reduced cytosolic p21/p27 retention, causing RhoA activation through positive feedback. Downregulation of p21/p27 by siRNA, and cytosolic p21/p27 by the nuclear export blocker leptomycin B, further reduced cell migration in the 3MC‐treated cells. Reduced cytosolic p21/p27 expr...
Source: Journal of Cellular Physiology - February 18, 2014 Category: Cytology Authors: Yung‐Ho Hsu, Chih‐Cheng Chang, Nian‐Jie Yang, Yi‐Hsuan Lee, Shu‐Hui Juan Tags: Original Research Article Source Type: research

Simvastatin prevents neuroinflammation by inhibiting N‐methyl‐D‐aspartic acid receptor 1 in 6‐hydroxydopamine‐treated PC12 cells
This study investigates the impact of simvastatin on neuroinflammation in experimental parkinsonian cell models. 6‐Hydroxydopamine (6‐OHDA)‐treated pheochromocytoma‐12 (PC12) cells were used to investigate the neuroprotective nature of simvastatin. After incubation with 6‐OHDA, simvastatin, and/or N‐methyl‐D‐aspartic acid receptor 1 (NMDAR1) siRNA for 24 hr, test kits were used to detect the levels of lactate dehydrogenase (LDH) and glutamate released from PC12 cells exposed to different culture media. The mRNA levels of tumor necrosis factor (TNF)‐α, interleukin (IL)−1β, and IL‐6 were determined by...
Source: Journal of Neuroscience Research - January 31, 2014 Category: Neuroscience Authors: Junqiang Yan, Jiachun Sun, Lina Huang, Qizhi Fu, Ganqin Du Tags: Research Article Source Type: research

Role of Claudin-5 in the Attenuation of Murine Acute Lung Injury by Simvastatin.
Abstract The statins are now recognized to have pleiotropic properties including augmentation of endothelial barrier function. To explore the mechanisms involved, we investigated the effect of simvastatin on endothelial cell (EC) tight junctions. Western blotting of human pulmonary artery EC treated with simvastatin (5 µM) confirmed a significant time-dependent increase (16-48 h) in claudin-5 protein expression compared to controls without detectable alterations in ZO-1 or occludin. These effects were associated with membrane translocation of VE-cadherin while knockdown of VE-cadherin (siRNA) inhibited simvastati...
Source: American Journal of Respiratory Cell and Molecular Biology - September 12, 2013 Category: Molecular Biology Authors: Chen W, Sharma R, Rizzo AN, Siegler JH, Garica JG, Jacobson JR Tags: Am J Respir Cell Mol Biol Source Type: research

Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway
Highlights: ► Lipophilic statin, simvastatin, triggers apoptosis in human breast cancer cells via JNK/CHOP/DR5 dependent signaling. ► Simvastatin blockage of mevalonate and geranylgeranyl pyrophosphate is critical for pro-death effect. ► Death Receptor 5 protein levels are upregulated by simvastatin and necessary for simvastatin-induced apoptosis.Abstract: Simvastatin (SVA) was shown to up-regulate expression of death receptor-5 (DR5), CCAAT/enhancer binding protein homologous protein (CHOP) and phosphorylated c-Jun N-terminal kinase (pJNK) in human breast cancer cell lines. siRNA knockdown of DR5, CHOP or JNK signif...
Source: Cancer Letters - December 7, 2012 Category: Cancer & Oncology Authors: Archana Gopalan, Weiping Yu, Bob G. Sanders, Kimberly Kline Tags: Research Articles Source Type: research