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Drug: Atorvastatin Calcium

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Total 38 results found since Jan 2013.

Self-amplified ROS production from fatty acid oxidation enhanced tumor immunotherapy by atorvastatin/PD-L1 siRNA lipopeptide nanoplexes
Biomaterials. 2022 Nov 3;291:121902. doi: 10.1016/j.biomaterials.2022.121902. Online ahead of print.ABSTRACTDespite the important role of reactive oxygen species (ROS) in battling cancer, ROS production with current approaches has been severely limited by the deficiency of oxy-substrates in tumor microenvironment. Herein, an atorvastatin (Ato)-catalytic self-amplified approach was utilized for sustainable ROS production and enhancing anti-tumor efficacy of PD-L1 silencing. A C18-pArg8-ss-pHis10 lipopeptide based self-assembled nanoplexes was developed to co-encapsulate AMP-activated protein kinase (AMPK) activator of Ato a...
Source: Biomaterials - November 13, 2022 Category: Materials Science Authors: Yan Gao Zilin Song Li Jia Yi Tang Chengcheng Wang Xiuli Zhao Haiyang Hu Dawei Chen Mingxi Qiao Source Type: research

Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch.
Abstract MURC (muscle-restricted coiled-coil protein) is a hypertrophy-related gene. Hypertrophy can be induced by mechanical stress. The purpose of this research was to investigate the hypothesis that MURC mediates hypertrophy in cardiomyocytes under mechanical stress. We used the in vivo model of an aortocaval shunt (AV shunt) in adult Wistar rats to induce myocardial hypertrophy. We also used the in vitro model of cyclic stretch in rat neonatal cardiomyocytes to clarify MURC expression and the molecular regulation mechanism. The flexible membrane culture plate seeding with cardiomyocytes Cardiomyocytes seeded o...
Source: J Cell Mol Med - December 3, 2018 Category: Molecular Biology Authors: Cheng WP, Lo HM, Wang BW, Chua SK, Shyu KG Tags: J Cell Mol Med 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 Inhibits Myocardial Apoptosis in a Swine Model of Coronary Microembolization by Regulating PTEN/PI3K/Akt Signaling Pathway
Conclusion: Modulation of PTEN was probably as a potential mechanism involved in the beneficial effects of pretreatment of atorvastatin to cardiac function and apoptosis in large animal models of CME.Cell Physiol Biochem 2016;38:207-219
Source: Cellular Physiology and Biochemistry - January 19, 2016 Category: Cytology Source Type: research

The anti ‑dengue virus properties of statins may be associated with alterations in the cellular antiviral profile expression.
The anti‑dengue virus properties of statins may be associated with alterations in the cellular antiviral profile expression. Mol Med Rep. 2016 Jul 13; Authors: Bryan-Marrugo OL, Arellanos-Soto D, Rojas-Martinez A, Barrera-Saldaña H, Ramos-Jimenez J, Vidaltamayo R, Rivas-Estilla AM Abstract Dengue virus (DENV) susceptibility to cholesterol depleting treatments has been previously reported. There are numerous questions regarding how DENV seizes cellular machinery and cholesterol to improve viral production and the effect of cholesterol sequestering agents on the cellular antiviral response. The aim of...
Source: Molecular Medicine Reports - July 21, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Atorvastatin alleviates cardiomyocyte apoptosis by suppressing TRB3 induced by acute myocardial infarction and hypoxia
Conclusion Treatment of atorvastatin inhibits the expression of TRB3 and cardiomyocyte apoptosis induced by AMI and hypoxia.
Source: Journal of the Formosan Medical Association - September 17, 2016 Category: Journals (General) Source Type: research

Atorvastatin alleviates cardiomyocyte apoptosis by suppressing TRB3 induced by acute myocardial infarction and hypoxia.
CONCLUSION: Treatment of atorvastatin inhibits the expression of TRB3 and cardiomyocyte apoptosis induced by AMI and hypoxia. PMID: 27645622 [PubMed - as supplied by publisher]
Source: J Formos Med Assoc - September 15, 2016 Category: Journals (General) Authors: Cheng WP, Lo HM, Wang BW, Chua SK, Lu MJ, Shyu KG Tags: J Formos Med Assoc Source Type: research

Effect of atorvastatin on LOX-1 and eNOS expression in collateral vessels of hypercholesterolemic rats.
CONCLUSIONS: Both hypercholesterolemia and oxLDL can induce endothelial dysfunction and impair collateral vessel growth via the LOX-1/eNOS pathway in rats, and atorvastatin treatment can restore the LOX-1/eNOS pathway to promote the growth of the collateral vessels, suggesting the potential of atorvastatin as a therapeutic agent to promote repair of collateral vessel injuries in ischemic diseases. PMID: 31852645 [PubMed - in process]
Source: Journal of Southern Medical University - November 29, 2019 Category: Universities & Medical Training Authors: Yinjuan T, Jianjun W, Yinglu G, Weijun C, Weijun T, Mingying L Tags: Nan Fang Yi Ke Da Xue Xue Bao 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

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.
Source: Biomedical and Environmental Sciences - November 9, 2014 Category: Biomedical Science 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-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