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Total 44 results found since Jan 2013.

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

Geranylgeraniol prevents the simvastatin-induced PCSK9 expression: Role of the small G protein Rac1
Publication date: August 2017 Source:Pharmacological Research, Volume 122 Author(s): Nicola Ferri, Silvia Marchianò, Maria Giovanna Lupo, Annalisa Trenti, Giuseppe Biondo, Paola Castaldello, Alberto Corsini Statins are known to increase the plasma levels of proprotein convertase subtilisin kexin type 9 (PCSK9) through the activation of the sterol responsive element binding protein (SREBP) pathway due to the inhibition of cholesterol biosynthesis. In the present study, we explore a possible role of the prenylated proteins on the statin-mediated PCSK9 induction in Caco-2 cells. Simvastatin (40μM) induced both PCSK9 mRNA (...
Source: Pharmacological Research - June 10, 2017 Category: Drugs & Pharmacology Source Type: research

Kruppel-like factor 4 (KLF-4) plays a crucial role in simvastatin (SVT)-induced differentiation of rabbit articular chondrocytes.
This study indicates that KLF-4 plays critical role in SVT-caused chondrocytes differentiation. PMID: 29775609 [PubMed - as supplied by publisher]
Source: Biochemical and Biophysical Research communications - May 15, 2018 Category: Biochemistry Authors: Yu SM, Kim SJ Tags: Biochem Biophys Res Commun Source Type: research

Simvastatin Protects Dopaminergic Neurons Against MPP < sup > + < /sup > -Induced Oxidative Stress and Regulates the Endogenous Anti-Oxidant System Through ERK
Conclusion: Our results provide strong evidence that ERK1/2-mediated modulation of the anti-oxidant system after simvastatin treatment may partially explain the anti-oxidant activity in experimental parkinsonian models. These findings contribute to a better understanding of the critical roles of simvastatin via the ERK1/2-mediated modulation of the anti-oxidant system, which may be relevant for treating PD.Cell Physiol Biochem 2018;51:1957 –1968
Source: Cellular Physiology and Biochemistry - December 4, 2018 Category: Cytology Source Type: research

Simvastatin preparations promote PDGF-BB secretion to repair LPS-induced endothelial injury through the PDGFR β/PI3K/Akt/IQGAP1 signalling pathway.
Simvastatin preparations promote PDGF-BB secretion to repair LPS-induced endothelial injury through the PDGFRβ/PI3K/Akt/IQGAP1 signalling pathway. J Cell Mol Med. 2019 Oct 01;: Authors: Zheng X, Zhang W, Wang Z Abstract Endothelial barrier dysfunction is a critical pathophysiological process of sepsis. Impaired endothelial cell migration is one of the main reasons for endothelial dysfunction. Statins may have a protective effect on endothelial barrier function. However, the effect and mechanism of statins on lipopolysaccharide (LPS)-induced endothelial barrier dysfunction remain unclear. Simvastatin ...
Source: J Cell Mol Med - September 30, 2019 Category: Molecular Biology Authors: Zheng X, Zhang W, Wang Z Tags: J Cell Mol Med 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

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

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

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

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
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

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

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

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

Inhibition of autophagy potentiates pemetrexed and simvastatin-induced apoptotic cell death in malignant mesothelioma and non-small cell lung cancer cells
In this study, we determined whether autophagy could be induced by pemetrexed and simvastatin cotreatment in malignant mesothelioma and NSCLC cells. Furthermore, we determined whether inhibition of autophagy drives apoptosis in malignant mesothelioma and NSCLC cells. Malignant mesothelioma MSTO-211H and A549 NSCLC cells were treated with pemetrexed and simvastatin alone and in combination to evaluate their effect on autophagy and apoptosis. Cotreatment with pemetrexed and simvastatin induced greater caspase-dependent apoptosis and autophagy than either drug alone in malignant mesothelioma and NSCLC cells. 3-Methyladenine (...
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Kim, H.-R., Cho, K.-H., Hwang, K.-E., Jeong, E.-T. Tags: 11.1 Lung Cancer Source Type: research