Mariana Deleanu
Romanian Academy
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Featured researches published by Mariana Deleanu.
Molecular Nutrition & Food Research | 2014
Camelia S. Stancu; Gabriela M. Sanda; Mariana Deleanu; Anca Volumnia Sima
SCOPE Hyperlipidemia, hyperglycemia, and the oxidative stress are among the known risk factors of atherosclerosis. Our aim was to assess the hypolipidemic and antioxidant effects of a probiotic mix (Lactobacillus acidophilus and Bifidobacterium animalis) in hyperlipidemic hamsters (HL). METHODS AND RESULTS Male Golden Syrian hamsters developed hyperlipidemia after 21 weeks of fat diet. For the last 5 weeks of experiment, ten HL were treated with the probiotic mix (HLP), ten received water (HL). Ten animals received standard chow (N). Increase of plasma total cholesterol (TC), triglycerides (TG), phospholipids (PL), oxidized LDL, glucose, of 4-hydroxynonenal (4-HNE) in plasma, liver, and myocardium, and of intestinal Niemann Pick C1 like 1 (NPC1L1) and microsomal TG transfer protein (MTTP) expression was observed in HL versus N. The probiotic mix decreased plasma TC, TG, PL, oxidized LDL, 4-HNE, and glucose levels and increased paraoxonase-1 activity, decreased NPC1L1 and MTTP protein expression compared to HL. In HLP liver, a significant reduction of TC, TG, and fatty acids was observed. PL increased and 4-HNE levels decreased in the liver and myocardium of HLP versus HL. CONCLUSION Our data support the administration of probiotics to humans because of their hypolipidemic (through decreasing intestinal NPC1L1 and MTTP) and antioxidant effects (stimulating HDL-associated paraoxonase-1).
European Journal of Pharmaceutics and Biopharmaceutics | 2015
Manuela Calin; Daniela Stan; Martin Schlesinger; Viorel Simion; Mariana Deleanu; Cristina Ana Constantinescu; Ana-Maria Gan; Monica Pirvulescu; Elena Butoi; Ileana Manduteanu; Marian Bota; Marius Enachescu; Lubor Borsig; Gerd Bendas; Maya Simionescu
Chemokines are critically involved in the development of chronic inflammatory-associated diseases such as atherosclerosis. We hypothesized that targeted delivery of compounds to the surface of activated endothelial cells (EC) interferes with chemokine/receptor interaction and thereby efficiently blocks inflammation. We developed PEGylated target-sensitive liposomes (TSL) encapsulating a CCR2 antagonist (Teijin compound 1) coupled with a specific peptide recognized by endothelial VCAM-1 (Vp-TSL-Tj). TSL were characterized for size (by dynamic light scattering), the amount of peptide coupled at the liposomal surface and Teijin release (by HPLC). We report that Vp-TSL-Tj binds specifically to activated EC in vitro and in situ, release the entrapped Teijin and prevent the transmigration of monocytes through activated EC. This is the first evidence that nanocarriers which transport and release chemokine inhibitors at specific pathological sites can reduce chemokine-dependent inflammatory processes.
Journal of Pharmacy and Pharmacology | 2016
Viorel Simion; Daniela Stan; Cristina Ana Constantinescu; Mariana Deleanu; Emanuel Dragan; Monica Madalina Tucureanu; Ana-Maria Gan; Elena Butoi; Alina Constantin; Ileana Manduteanu; Maya Simionescu; Manuela Calin
To prepare and characterize in vitro and in vivo lipid nanoemulsions (LN) loaded with curcumin (Cm) and functionalized with a cell‐penetrating peptide.
Molecular Nutrition & Food Research | 2015
Camelia S. Stancu; Mihaela G. Carnuta; Gabriela M. Sanda; Laura Toma; Mariana Deleanu; Loredan S. Niculescu; Shlomo Sasson; Maya Simionescu; Anca V. Sima
SCOPE We aimed at investigating the mechanisms linking hyperlipidemia (HL) with dysfunctional HDL and its main antioxidant enzyme, paraoxonase1 (PON1). PON1 expression and activity was determined in the small intestine, liver, and sera of normal and HL hamsters and associated with the ER stress (ERS) and the development of aortic valve lesions. METHODS AND RESULTS Male Golden Syrian hamsters were fed standard chow (N) or standard diet with 3% cholesterol and 15% butter for 16 weeks. All hamsters on fat diet developed HL, 50% also hyperglycemia (HLHG) and a fourfold increased homeostasis model assessment of insuline resistance. PON1 expression was reduced in the small intestine and liver (N > HL > HLHG) along with the increased extent of ERS, oxidized lipids, and decreased expression of liver X receptors beta (LXRβ) in the small intestine, peroxisome proliferator-activated receptor-γ (PPARγ) in the liver, and of the glucose transporter 4 in the myocardium. Serum PON1 levels decreased along with the increase of oxidized LDL and lesion areas of the aortic valves (N > HL > HLHG). CONCLUSION The fat diet activates the ERS and oxidative stress, decreases LXRβ, PPARγ, and PON1 in the small intestine, liver, and sera of all HL animals, in parallel with the appearance of atherosclerotic lesions in the aortic valves.
Scientific Reports | 2017
Mihaela G. Carnuta; Camelia S. Stancu; Laura Toma; Gabriela M. Sanda; Loredan S. Niculescu; Mariana Deleanu; Andreea C. Popescu; Mihaela R. Popescu; Adelina Vlad; Doina R. Dimulescu; Maya Simionescu; Anca V. Sima
There is a stringent need to find means for risk stratification of coronary artery diseases (CAD) patients. We aimed at identifying alterations of plasma high-density lipoproteins (HDL) components and their validation as dysfunctional HDL that could discriminate between acute coronary syndrome (ACS) and stable angina (SA) patients. HDL2 and HDL3 were isolated from CAD patients’ plasma and healthy subjects. ApolipoproteinAI (apoAI), apoAII, apoCIII, malondialdehyde (MDA), myeloperoxidase (MPO), ceruloplasmin and paraoxonase1 (PON1) were assessed. The anti-inflammatory potential of HDL subfractions was tested by evaluating the secreted inflammatory molecules of tumor necrosis factor α-activated endothelial cells (EC) upon co-incubation with HDL2 or HDL3. We found in ACS versus SA patients: 40% increased MPO, MDA, apoCIII in HDL2 and HDL3, 35% augmented apoAII in HDL2, and in HDL3 increased ceruloplasmin, decreased apoAII (40%) and PON1 protein and activity (15% and 25%). Co-incubation of activated EC with HDL2 or HDL3 from CAD patients induced significantly increased levels of secreted inflammatory molecules, 15–20% more for ACS versus SA. In conclusion, the assessed panel of markers correlates with the reduced anti-inflammatory potential of HDL subfractions isolated from ACS and SA patients (mostly for HDL3 from ACS) and can discriminate between these two groups of CAD patients.
Journal of Cellular Biochemistry | 2017
Gabriela M. Sanda; Mariana Deleanu; Laura Toma; Camelia S. Stancu; Maya Simionescu; Anca V. Sima
Oxidatively modified low‐density lipoproteins (oxLDL) alter the proper function of the endoplasmic reticulum (ER), inducing ER stress (ERS), which consequently activates inflammatory pathways in macrophages. Matrix metalloproteinase‐9 (MMP‐9) is the main protease acting on the degradation of the extracellular matrix and the ensuing destabilization of the atherosclerotic plaque. We aimed to investigate whether ERS induced by oxLDL or tunicamycin (TM) in human macrophages is associated with the stimulation of MMP‐9 expression and secretion. The results showed that oxLDL induced in THP‐1 macrophages: (i) increase of MMP‐9 gene expression and its pro‐form secretion, (ii) intracellular accumulation of 7‐ketocholesterol, (iii) ERS activation (increased eIF2α phosphorylation, XBP1 and CHOP mRNA levels, and Grp78 protein expression), and (iv) oxidative stress (increased levels of reactive oxygen species and NADPH oxidase activity). Incubation of macrophages with ERS inducer, TM determined the secretion of both pro‐ and active‐form of MMP‐9 and oxidative stress. Treatment of oxLDL or TM‐incubated cells with ERS inhibitor, sodium phenylbutyrate decreased MMP‐9 gene expression, secretion, and activity. The inhibitor of NADPH oxidase, apocynin, decreased XBP‐1 and CHOP mRNA levels, and MMP‐9 gene expression and secretion in oxLDL‐exposed cells. In conclusion, oxLDL stimulate MMP‐9 expression and secretion in human macrophages by mechanisms involving ERS. J. Cell. Biochem. 118: 661–669, 2017.
Biofactors | 2017
Laura Toma; Gabriela M. Sanda; Loredan S. Niculescu; Mariana Deleanu; Camelia S. Stancu; Anca V. Sima
Type 2 diabetes mellitus is a worldwide epidemic and its atherosclerotic complications determine the high morbidity and mortality of diabetic patients. Caffeic acid (CAF), a phenolic acid present in normal diets, is known for its antioxidant properties. The aim of this study was to investigate CAFs anti-inflammatory properties and its mechanism of action, using cultured human endothelial cells (HEC) incubated with glycated low-density lipoproteins (gLDL). Levels of the receptor for advanced glycation end-products (RAGE), inflammatory stress markers (C reactive protein, CRP; vascular cell adhesion molecule-1, VCAM-1; monocyte chemoattractant protein-1, MCP-1), and oxidative stress and endoplasmic reticulum stress (ERS) markers were evaluated in gLDL-exposed HEC, in the presence/absence of CAF. RAGE silencing or blocking, specific inhibitors for oxidative stress (apocynin, N-acetyl-cysteine), and ERS (salubrinal) were used. The results showed that: (i) gLDL induced CRP synthesis and secretion through mechanisms involving NADPH oxidase-dependent oxidative stress and ERS in HEC; (ii) gLDL-RAGE interaction, oxidative stress, and ERS stimulated the secretion of VCAM-1 and MCP-1 in HEC; and (iii) CAF reduced the secretion of CRP, VCAM-1, and MCP-1 in gLDL-exposed HEC by inhibiting RAGE expression, oxidative stress, and ERS. In conclusion, CAF might be a promising alternative to ameliorate a wide spectrum of disorders due to its complex mechanisms of action resulting in anti-inflammatory and antioxidative properties.
International Journal of Nanomedicine | 2017
Monica Madalina Tucureanu; Daniela Rebleanu; Cristina Ana Constantinescu; Mariana Deleanu; Geanina Voicu; Elena Butoi; Manuela Calin; Ileana Manduteanu
Background Lipopolysaccharide (LPS) is widely recognized as a potent activator of monocytes/macrophages, and its effects include an altered production of key mediators, such as inflammatory cytokines and chemokines. The involvement of Gi protein in mediating LPS effects has been demonstrated in murine macrophages and various cell types of human origin. Purpose The aim of the present work was to evaluate the potential of a Gi-protein inhibitor encapsulated in liposomes in reducing the inflammatory effects induced by LPS in monocytes/macrophages. Materials and methods Guanosine 5′-O-(2-thiodiphosphate) (GOT), a guanosine diphosphate analog that completely inhibits G-protein activation by guanosine triphosphate and its analogs, was encapsulated into liposomes and tested for anti-inflammatory effects in LPS-activated THP1 monocytes or THP1-derived macrophages. The viability of monocytes/macrophages after incubation with different concentrations of free GOT or liposome-encapsulated GOT was assessed by MTT assay. MAPK activation and production of IL1β, TNFα, IL6, and MCP1 were assessed in LPS-activated monocytes/macrophages in the presence or absence of free or encapsulated GOT. In addition, the effect of free or liposome-encapsulated GOT on LPS-stimulated monocyte adhesion to activated endothelium and on monocyte chemotaxis was evaluated. Results We report here that GOT-loaded liposomes inhibited activation of MAPK and blocked the production of the cytokines IL1β, TNFα, IL6, and MCP1 induced by LPS in monocytes and macrophages. Moreover, GOT encapsulated in liposomes reduced monocyte adhesion and chemotaxis. All demonstrated events were in contrast with free GOT, which showed reduced or no effect on monocyte/macrophage activation with LPS. Conclusion This study demonstrates the potential of liposomal GOT in blocking LPS proinflammatory effects in monocytes/macrophages.
Molecular and Cellular Biochemistry | 2016
Laura Toma; Gabriela M. Sanda; Mariana Deleanu; Camelia S. Stancu; Anca V. Sima
Journal of Nanoparticle Research | 2013
Viorel Simion; Daniela Stan; Ana-Maria Gan; Monica Pirvulescu; Elena Butoi; Ileana Manduteanu; Mariana Deleanu; Eugen Andrei; Anamaria Durdureanu-Angheluta; Marian Bota; Marius Enachescu; Manuela Calin; Maya Simionescu