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Drug: Atorvastatin Calcium

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Total 38 results found since Jan 2013.

Atorvastatin restricts HIV replication in CD4+ T cells by upregulation of p21
Conclusion: The results demonstrate a novel mechanism by which atorvastatin induced resistance of CD4+ T cells to HIV-1 infection via p21 upregulation and suggest that statins may hold particular promise for some HIV-infected individuals.
Source: AIDS - December 23, 2015 Category: Infectious Diseases Tags: Basic Science Source Type: research

Involvement of Pregnane X Receptor in the Impaired Glucose Utilization Induced by Atorvastatin in Hepatocytes.
In conclusion, atorvastatin impaired glucose utilization in hepatocytes via repressing GLUT2 and GCK expressions, which may be partly due to PXR activation. PMID: 26616219 [PubMed - as supplied by publisher]
Source: Biochemical Pharmacology - November 23, 2015 Category: Drugs & Pharmacology Authors: Ling Z, Shu N, Xu P, Wang F, Zhong Z, Sun B, Li F, Zhang M, Zhao K, Tang X, Wang Z, Zhu L, Liu L, Liu X Tags: Biochem Pharmacol 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

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

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

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

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