scholarly journals Tyrosol May Prevent Obesity by Inhibiting Adipogenesis in 3T3-L1 Preadipocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Francesca Pacifici ◽  
Carolina Lane Alves Farias ◽  
Silvia Rea ◽  
Barbara Capuani ◽  
Alessandra Feraco ◽  
...  

Tyrosol (TR), a major polyphenol found in extra virgin olive oil (EVOO), exerts several antioxidant effects. However, only scarce evidences are present regarding its activity on adipocytes and obesity. This study evaluated the role of TR in adipogenesis. Murine 3T3-L1 preadipocytes were incubated with TR (300 and 500 μM), and TR administration inhibited adipogenesis by downregulation of several adipogenic factors (leptin and aP2) and transcription factors (C/EBPα, PPARγ, SREBP1c, and Glut4) and by modulation of the histone deacetylase sirtuin 1. After complete differentiation, adipocytes treated with 300 and 500 μM TR showed a reduction of 20% and 30% in lipid droplets, respectively. Intracellular triglycerides were significantly reduced after TR treatment ( p < 0.05 ). Mature adipocytes treated with TR at 300 and 500 μM showed a marked decrease in the inflammatory state and oxidative stress as shown by the modulation of specific biomarkers (TNF, IL6, ROS, and SOD2). TR treatment also acted on the early stage of differentiation by reducing cell proliferation (~40%) and inducing cell cycle arrest during Mitotic Expansion Clonal (first 48 h of differentiation), as shown by the increase in both S1 phase and p21 protein expression. We also showed that TR induced lipolysis by activating the AMPK-ATGL-HSL pathway. In conclusion, we provided evidence that TR reduces 3T3-L1 differentiation through downregulation of adipogenic proteins, inflammation, and oxidative stress. Moreover, TR may trigger adipose tissue browning throughout the induction of the AMPK-ATGL-UCP1 pathway and, subsequently, may have promise as a potential therapeutic agent for the treatment and prevention of obesity.

2012 ◽  
Vol 15 (6) ◽  
pp. 601-612 ◽  
Author(s):  
Vanessa Pitozzi ◽  
Michela Jacomelli ◽  
Dolores Catelan ◽  
Maurizio Servili ◽  
Agnese Taticchi ◽  
...  

Nutrition ◽  
2021 ◽  
pp. 111270
Author(s):  
Lorenzo Loffredo ◽  
Maria Del Ben ◽  
Simona Bartimoccia ◽  
Valentina Castellani ◽  
Mirta Mancinella ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Hicham Berrougui ◽  
Souad Ikhlef ◽  
Abdelouahed Khalil

Results of the present work give evidence from the beneficial role of extra virgin olive of oil (EVOO) consumption towards oxidative stress and cardiovascular diseases. Polyphenols contained in EVOO are responsible for inhibiting lipoproteins oxidative damages and promoting reverse cholesterol transport process via ABCA1 pathway.


2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Annalisa Noce ◽  
Francesca Di Daniele ◽  
Giulia Marrone ◽  
Anna Pietroboni Zaitseva ◽  
Silvia Urciuoli ◽  
...  

Abstract Background and Aims Chronic degenerative non-communicable diseases represent one of the main causes of death in the world. Among these, chronic kidney disease (CKD) has an estimated prevalence of 7-12% worldwide. CKD is related to numerous comorbidities, especially these cardiovascular. Furthermore, its progression is characterized by a low-grade inflammatory status and oxidative stress, factors that negatively influence quality of life. In recent years, numerous in vitro and in vivo studies have analysed the beneficial effects of natural bioactive compounds on health. Extra virgin olive oil (EVOO) is rich in minor polar compounds (MPCs), capable of exerting a cardioprotective, anti-inflammatory and antioxidant action. The 98-99% of EVOO total weight is made up by fatty acids, in particular, monounsaturated ones such as oleic acid, and a small percentage 1-2% by MPCs. Among MPCs, hydroxytyrosol, tyrosol, oleacin and oleocanthal are of particular importance for their heathy effects. In our study, we analysed the potential healthy effects of EVOO MPCs in CKD patients. Method The EVOO selected for the study (Ophenoil), was previously characterized for its high content of MPCs through quantitative and qualitative analysis performed using HPLC-DAD-MS and Oxitester. We enrolled 20 CKD patients undergoing conservative therapy (stages I-IV according to K-DIGO guidelines). All enrolled patients have been instructed to assume 40 ml per day of EVOO, for 9 weeks. Laboratory parameters have been collected at two different time-points of the study (at baseline T0 and after 9 weeks T1) (Fig 1). At T0 the patients have been undergo to a detailed medical history. All CKD patients have been unstructured to follow a conventional Mediterranean diet (which adherence is assessed by PREDIMED questionnaire), containing a controlled protein intake according to CKD stage, in which the EVOO Ophenoil represent the main source of plant-based fats. In both time-points of the study, all patients have been undergoing to blood sampling to evaluate renal function, lipid profile, inflammatory parameters (C-reactive protein-CRP, erythrocyte sedimentation rate-ESR, Interleukin(IL)-6, Tumor necrosis factor(TNF)-α) and oxidative stress (Free Oxygen Radicals Test-FORT and Free Oxygen Radical Defence-FORD by CR4000). Moreover, we evaluated the cardiovascular risk indices (Carotid intima-Media Thickness (C-ITM) monitored by eco(color)Doppler ultrasound). Each patient has been interviewed with Quality of Life Assessment Questionnaire (Short-Form 36 items health Survey- SF-36) and International Physical Activity Questionnaire (IPAQ). Results Preliminary data highlight a reduction of the inflammatory state, monitored by CRP (p=0.0299), ESR (p=0.0063), TNF-α (p=0.0001), IL-6 (p=0.0219), an improvement of renal function (azotemia, p=0.0256) and of lipid profile (triglycerides, p=0.0476) after 9 weeks of EVOO assumption (Fig 2). Moreover, we observed a significant improvement of the C-ITM (p=0.0146) and a significant reduction of oxidative stress monitored by FORT (p=0.0144). The results of the PREDIMED and IPAQ questionnaires showed no significant differences. This data indicates that patients have not changed their lifestyle and the results obtained are attributable to EVOO assumption. At the end of the study, there was an improvement of quality of life, in the domains of emotional well-being (p=0.0340) and general health (p=0.0405) of SF-36 questionnaire (Fig 3). Conclusion The consumption of EVOO with high MPCs content would seem to exert an anti-inflammatory (due to high content of oleocanthal) and antioxidant (due to high content of hydroxytyrosol, oleacin and oleuropein aglicone) action in CKD patients. Therefore, once again it is highlighted how the diet therapy plays a pivotal role in the clinical management of CKD patients and that it allows an improvement of their quality of life.


Nutrition ◽  
2015 ◽  
Vol 31 (6) ◽  
pp. 834-840 ◽  
Author(s):  
Danielle Venturini ◽  
Andréa Name Colado Simão ◽  
Mariana Ragassi Urbano ◽  
Isaias Dichi

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.


2020 ◽  
Vol 17 (4) ◽  
pp. 394-401
Author(s):  
Yuanhua Wu ◽  
Yuan Huang ◽  
Jing Cai ◽  
Donglan Zhang ◽  
Shixi Liu ◽  
...  

Background: Ischemia/reperfusion (I/R) injury involves complex biological processes and molecular mechanisms such as autophagy. Oxidative stress plays a critical role in the pathogenesis of I/R injury. LncRNAs are the regulatory factor of cerebral I/R injury. Methods: This study constructs cerebral I/R model to investigate role of autophagy and oxidative stress in cerebral I/R injury and the underline regulatory mechanism of SIRT1/ FOXO3a pathway. In this study, lncRNA SNHG12 and FOXO3a expression was up-regulated and SIRT1 expression was down-regulated in HT22 cells of I/R model. Results: Overexpression of lncRNA SNHG12 significantly increased the cell viability and inhibited cerebral ischemicreperfusion injury induced by I/Rthrough inhibition of autophagy. In addition, the transfected p-SIRT1 significantly suppressed the release of LDH and SOD compared with cells co-transfected with SIRT1 and FOXO3a group and cells induced by I/R and transfected with p-SNHG12 group and overexpression of cells co-transfected with SIRT1 and FOXO3 further decreased the I/R induced release of ROS and MDA. Conclusion: In conclusion, lncRNA SNHG12 increased cell activity and inhibited oxidative stress through inhibition of SIRT1/FOXO3a signaling-mediated autophagy in HT22 cells of I/R model. This study might provide new potential therapeutic targets for further investigating the mechanisms in cerebral I/R injury and provide.


2013 ◽  
Vol 8 (4) ◽  
pp. 266-277 ◽  
Author(s):  
Diego Duarte ◽  
Kamila Silva ◽  
Mariana Rosales ◽  
José Lopes de Faria ◽  
Jacqueline Lopes de Faria

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3314
Author(s):  
Tomasz Kowalczyk ◽  
Joanna Kisluk ◽  
Karolina Pietrowska ◽  
Joanna Godzien ◽  
Miroslaw Kozlowski ◽  
...  

Identification of the NSCLC subtype at an early stage is still quite sophisticated. Metabolomics analysis of tissue and plasma of NSCLC patients may indicate new, and yet unknown, metabolic pathways active in the NSCLC. Our research characterized the metabolomics profile of tissue and plasma of patients with early and advanced NSCLC stage. Samples were subjected to thorough metabolomics analyses using liquid chromatography-mass spectrometry (LC-MS) technique. Tissue and/or plasma samples from 137 NSCLC patients were analyzed. Based on the early stage tissue analysis, more than 200 metabolites differentiating adenocarcinoma (ADC) and squamous cell lung carcinoma (SCC) subtypes as well as normal tissue, were identified. Most of the identified metabolites were amino acids, fatty acids, carnitines, lysoglycerophospholipids, sphingomyelins, plasmalogens and glycerophospholipids. Moreover, metabolites related to N-acyl ethanolamine (NAE) biosynthesis, namely glycerophospho (N-acyl) ethanolamines (GP-NAE), which discriminated early-stage SCC from ADC, have also been identified. On the other hand, the analysis of plasma of chronic obstructive pulmonary disease (COPD) and NSCLC patients allowed exclusion of the metabolites related to the inflammatory state in lungs and the identification of compounds (lysoglycerophospholipids, glycerophospholipids and sphingomyelins) truly characteristic to cancer. Our results, among already known, showed novel, thus far not described, metabolites discriminating NSCLC subtypes, especially in the early stage of cancer. Moreover, the presented results also indicated the activity of new metabolic pathways in NSCLC. Further investigations on the role of NAE biosynthesis pathways in the early stage of NSCLC may reveal new prognostic and diagnostic targets.


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