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Total 179 results found since Jan 2013.

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

Atorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglin.
Authors: Zemankova L, Varejckova M, Dolezalova E, Fikrova P, Jezkova K, Rathouska J, Cerveny L, Botella LM, Bernabeu C, Nemeckova I, Nachtigal P Abstract Endoglin, a transforming growth factor β (TGF-β) receptor type III, is co-expressed with endothelial nitric oxide synthase (eNOS) in aortic endothelium in atherosclerotic plaques of mice. Interestingly, atorvastatin (ATV) is able to increase both endoglin and eNOS expression and reduce plaque size beyond its lipid lowering effects but by unknown mechanisms. We hypothesized whether inflammation modulates ATV-dependent induction of endoglin and eNOS expression in ...
Source: Journal of Physiology and Pharmacology - June 20, 2015 Category: Drugs & Pharmacology Tags: J Physiol Pharmacol 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

Atorvastatin attenuates homocysteine-induced migration of smooth muscle cells through mevalonate pathway involving reactive oxygen species and p38 MAPK.
This article is protected by copyright. All rights reserved. PMID: 26041506 [PubMed - as supplied by publisher]
Source: Clinical and Experimental Pharmacology and Physiology - June 4, 2015 Category: Drugs & Pharmacology Authors: Bao XM, Zheng H Tags: Clin Exp Pharmacol Physiol Source Type: research

New CETP Inhibitor K-312 Reduces PCSK9 Expression: A Potential Effect on LDL Cholesterol Metabolism.
Abstract Despite significant reduction of cardiovascular events by statin treatment, substantial residual risk persists, driving emerging needs for the development of new therapies. We identified a novel cholesteryl ester transfer protein (CETP) inhibitor, K-312, that raises HDL- and lowers LDL-cholesterol levels in animals. K-312 also suppresses hepatocyte expression of proprotein convertase subtilisin/kexin 9 (PCSK9), a molecule that increases LDL cholesterol. We explored the underlying mechanism for the reduction of PCSK9 expression by K-312. K-312 inhibited in vitro human plasma CETP activity (IC50: 0.06 μM)....
Source: Am J Physiol Endocri... - May 26, 2015 Category: Endocrinology Authors: Miyosawa K, Watanabe Y, Murakami K, Murakami T, Shibata H, Iwashita M, Yamazaki H, Yamazaki K, Ohgiya T, Shibuya K, Mizuno K, Tanabe S, Singh SA, Aikawa M Tags: Am J Physiol Endocrinol Metab Source Type: research

Atorvastatin reduces long pentraxin 3 expression in vascular cells by inhibiting protein geranylgeranylation.
CONCLUSIONS: Results suggest that statins may interfere with PTX3 expression in vascular cells via inhibition of protein geranylgeranylation. Since PTX3 is increasingly regarded as an important mediator of the inflammatory response underlying atherosclerosis and its complications, these results highlight the need for further studies of the role of PTX3 and its potential pharmacological modulation in cardiovascular disease. PMID: 25849951 [PubMed - as supplied by publisher]
Source: Vascular Pharmacology - April 4, 2015 Category: Drugs & Pharmacology Authors: Baetta R, Lento S, Ghilardi S, Barbati E, Corsini A, Tremoli E, Banfi C Tags: Vascul Pharmacol Source Type: research

Statins meditate anti-atherosclerotic action in smooth muscle cells by peroxisome proliferator-activated receptor-γ activation.
Abstract The peroxisome proliferator-activated receptor-γ (PPARγ) is an important regulator of lipid and glucose metabolism, and its activation is reported to suppress the progression of atherosclerosis. We have reported that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) activate PPARγ in macrophages. However, it is not yet known whether statins activate PPARγ in other vascular cells. In the present study, we investigated whether statins activate PPARγ in smooth muscle cells (SMCs) and endothelial cells (ECs) and thus mediate anti-atherosclerotic effects. Human aortic SMCs (HASMCs) and ...
Source: Biochemical and Biophysical Research communications - December 18, 2014 Category: Biochemistry Authors: Fukuda K, Matsumura T, Senokuchi T, Ishii N, Kinoshita H, Yamada S, Murakami S, Nakao S, Motoshima H, Kondo T, Kukidome D, Kawasaki S, Kawada T, Nishikawa T, Araki E Tags: Biochem Biophys Res Commun Source Type: research

Statin Inhibits the Expression of Secretory Phospholipase A2 and Subsequent Monocyte Chemoattractant Protein-1 in Human Endothelial Cells
We reported that tumor necrosis factor-alpha (TNFα) enhanced the expression of group V PLA2 (sPLA2-V) in human umbilical vein endothelial cells (HUVECs), and the LPC content in LDL and the monocyte chemoattractant protein-1 (MCP-1) expression were augmented when TNFα-stimulated HUVECs were incubated with LDL. Here, we observed that an HMG-CoA reductase inhibitor, pitavastatin, at the concentration of>1 μM administered 12 hours before TNFα stimulation suppressed the enhancement of sPLA2-V mRNA and protein. Pitavastatin also prevented the enhancement of the LPC content in LDL and the expression of MCP-1 mRNA when TNFα-s...
Source: Journal of Cardiovascular Pharmacology - December 1, 2014 Category: Cardiology Tags: Original Article 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

Atorvastatin Attenuates TNF-alpha Production via Heme Oxygenase-1 Pathway in LPS-stimulated RAW264.7 Macrophages
Conclusion Atorvastatin can attenuate LPS-induced TNF-α expression and production by activating HO-1 via the ERK and p38 MAPK pathways, suggesting that atorvastatin can be used in treatment of inflammatory diseases such as sepsis, especially in those with atherosclerotic diseases.
Source: Biomedical and Environmental Sciences - November 9, 2014 Category: Biomedical Science Source Type: research

Statins upregulate cystathionine γ-lyase transcription and H2S generation via activating Akt signaling in macrophage
In this study, we examined the effects of three different statins (fluvastatin, atorvastatin and pravastatin) on H2S formation in raw264.7 macrophages. There was a remarkable rise in H2S level in fluvastatin- and atorvastatin-stimulated macrophages, while pravastatin failed to show any significant effect on it. Moreover, fluvastatin and atorvastatin enhanced the mRNA and protein expression of cystathionine γ-lyase (CSE) in dose- and time-dependent manners. Fluvastatin also markedly enhanced the CSE activity. However, fluvastatin did not alter the mRNA or protein expression of another H2S-producing enzyme 3-mercaptopyruvat...
Source: Pharmacological Research - November 6, 2014 Category: Drugs & Pharmacology 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

Atorvastatin Attenuates TNF-alpha Production via Heme Oxygenase-1 Pathway in LPS-stimulated RAW264.7 Macrophages.
CONCLUSION: Atorvastatin can attenuate LPS-induced TNF-α expression and production by activating HO-1 via the ERK and p38 MAPK pathways, suggesting that atorvastatin can be used in treatment of inflammatory diseases such as sepsis, especially in those with atherosclerotic diseases. PMID: 25341814 [PubMed - in process]
Source: Biomedical and Environmental Sciences : BES - October 1, 2014 Category: Biomedical Science Authors: Wang XQ, Luo NS, Salah ZQ, Lin YQ, Gu MN, Chen YX Tags: Biomed Environ Sci Source Type: research