scholarly journals Quercetin Prevents Diastolic Dysfunction Induced by a High-Cholesterol Diet: Role of Oxidative Stress and Bioenergetics in Hyperglycemic Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Rodrigo L. Castillo ◽  
Emilio A. Herrera ◽  
Alejandro Gonzalez-Candia ◽  
Marjorie Reyes-Farias ◽  
Nicole de la Jara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diastolic Dysfunction ◽  
Nuclear Translocation ◽  
High Cholesterol Diet ◽  
High Cholesterol ◽  
Functional Changes ◽  
Cardioprotective Effects ◽  
Antioxidant Mechanisms ◽  
Antioxidant Enzymatic Activity

Alterations in cardiac energy metabolism play a key role in the pathogenesis of diabetic cardiomyopathy. Hypercholesterolemia associated with bioenergetic impairment and oxidative stress has not been well characterized in the cardiac function under glycemic control deficiency conditions. This work aimed to determine the cardioprotective effects of quercetin (QUE) against the damage induced by a high-cholesterol (HC) diet in hyperglycemic rats, addressing intracellular antioxidant mechanisms and bioenergetics. Quercetin reduced HC-induced alterations in the lipid profile and glycemia in rats. In addition, QUE attenuated cardiac diastolic dysfunction (increased E:A ratio), prevented cardiac cholesterol accumulation, and reduced the increase in HC-induced myocyte density. Moreover, QUE reduced HC-induced oxidative stress by preventing the decrease in GSH/GSSG ratio, Nrf2 nuclear translocation, HO-1 expression, and antioxidant enzymatic activity. Quercetin also counteracted HC-induced bioenergetic impairment, preventing a reduction in ATP levels and alterations in PGC-1α, UCP2, and PPARγ expression. In conclusion, the mechanisms that support the cardioprotective effect of QUE in rats with HC might be mediated by the upregulation of antioxidant mechanisms and improved bioenergetics on the heart. Targeting bioenergetics with QUE can be used as a pharmacological approach to modulate structural and functional changes of the heart under hypercholesterolemic and hyperglycemic conditions.

scholarly journals Potential role of nuclear translocation of glyceraldehyde-3-phosphate dehydrogenase in apoptosis and oxidative stress

2001 ◽  
Vol 114 (9) ◽  
pp. 1643-1653 ◽  
Author(s):  
Z. Dastoor ◽  
J.L. Dreyer
Keyword(s):  
Oxidative Stress ◽  
Laser Scanning ◽  
Fluorescent Protein ◽  
Nuclear Translocation ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Apoptotic Cells ◽  
Transfected Cells ◽  
And Oxidative Stress

Recent studies indicating a role of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in apoptosis or oxidative stress has been reported. Using confocal laser-scanning microscopy, we have investigated the cellular distribution of GAPDH in central nervous system (CNS)-derived cells (neuroblastoma mNB41A3), in non-CNS derived cells (R6 fibroblast) and in an apoptosis-resistant Bcl2 overexpressing cell line (R6-Bcl2). Induction of apoptosis by staurosporine or MG132 and oxidative stress by H(2)O(2) or FeCN enhanced the nuclear translocation of endogenous GAPDH in all cell types, as detected by immunocytochemistry. In apoptotic cells, GAPDH expression is three times higher than in non-apoptotic cells. Consistent with a role for GAPDH in apoptosis, overexpression of a GAPDH-green fluorescent protein (GAPDH-GFP) hybrid increased nuclear import of GAPDH-GFP into transfected cells and the number of apoptotic cells, and made them more sensitive to agents that induce apoptosis. Bcl2 overexpression prevents nuclear translocation of GAPDH and apoptosis in untransfected cells, but not in transfected cells that overexpress GAPDH-GFP. Our observations indicate that nuclear translocation of GAPDH may play a role in apoptosis and oxidative stress, probably related to the activity of GAPDH as a DNA repair enzyme or as a nuclear carrier for pro-apoptotic molecules.

Role of Thiol-Disulfide System in Mechanisms of Functional Changes in Neutrophils under Conditions of Oxidative Stress

2010 ◽  
Vol 150 (2) ◽  
pp. 198-202
Author(s):  
E. A. Stepovaya ◽  
G. V. Petina ◽  
T. V. Zhavoronok ◽  
N. V. Ryazanceva ◽  
V. V. Ivanov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Functional Changes

PPARβ/δ Priming Enhances the Anti-Apoptotic and Therapeutic Properties of Mesenchymal Stromal Cells in Myocardial Ischemia-Reperfusion Injury

2021 ◽  
Author(s):  
Charlotte Sarre ◽  
Rafael Contreras Lopez ◽  
Nitirut Nerpernpisooth ◽  
Christian Barrere ◽  
Sarah Bahraoui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Ex Vivo ◽  
Phase Iii ◽  
Therapeutic Properties ◽  
Cardioprotective Effects

Abstract Background: Mesenchymal Stromal Cells (MSC) have been widely used for their therapeutic properties in many clinical applications including myocardial infarction. Despite promising preclinical results and evidences of safety and efficacy in phases I/ II, inconsistencies in phase III trials have been reported. In a previous study, we have shown using MSC derived from the bone marrow of PPARβ/δ (Peroxisome proliferator-activated receptors β/δ) knockout mice that the acute cardioprotective properties of MSC during the first hour of reperfusion are PPARβ/δ-dependent but not related to the anti-inflammatory effect of MSC. However, the role of the modulation of PPARβ/δ expression on MSC cardioprotective and anti-apoptotic properties has never been investigated. Objectives: The aim of this study was to investigate the role of PPARβ/δ modulation (inhibition or activation) in MSC therapeutic properties in vitro and ex vivo in an experimental model of myocardial infarction.Methods and results: Naïve MSC and MSC pharmacologically activated or inhibited for PPARβ/δ were challenged with H202. Through specific DNA fragmentation quantification and qRT-PCR experiments, we evidenced in vitro an increased resistance to oxidative stress in MSC pre-treated by the PPARβ/δ agonist GW0742 versus naïve MSC. In addition, PPARβ/δ-priming allowed to reveal the anti-apoptotic effect of MSC on co-cultured cardiomyocytes. When injected during reperfusion in an ex vivo heart model of myocardial infarction, PPARβ/δ-primed MSC at a dose of 3.75x105 MSC/heart provided the same cardioprotective efficiency than 7.5x105 naïve MSC, identified as the optimal dose in our model. These enhanced short-term cardioprotective effects were associated with an increase in both anti-apoptotic effects and the number of MSC detected in the left ventricular wall at 1 hour of reperfusion. By contrast, inhibition of PPARβ/δ before their administration in post-ischemic hearts during reperfusion decreased their cardioprotective effects. Conclusion: Altogether these results revealed that PPARβ/δ-primed MSC exhibit an increased resistance to oxidative stress and enhanced anti-apoptotic properties on cardiac cells in vitro. PPARβ/δ-priming appears as an innovative strategy to enhance the cardioprotective effects of MSC and to decrease the injected doses. These results could be of major interest to improve MSC efficacy for the cardioprotection of injured myocardium in AMI patients.

scholarly journals Cardioprotective Effects of Dietary Phytochemicals on Oxidative Stress in Heart Failure by a Sex-Gender-Oriented Point of View

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Klara Komici ◽  
Valeria Conti ◽  
Sergio Davinelli ◽  
Leonardo Bencivenga ◽  
Giuseppe Rengo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Point Of View ◽  
World Population ◽  
Efficacy And Safety ◽  
Innovative Strategy ◽  
Dietary Phytochemicals ◽  
Clinical Models ◽  
Cardioprotective Effects ◽  
Therapeutic Tools

Dietary phytochemicals are considered an innovative strategy that helps to reduce cardiovascular risk factors. Some phytochemicals have been shown to play a beneficial role in lipid metabolism, to improve endothelial function and to modify oxidative stress pathways in experimental and clinical models of cardiovascular impairment. Importantly, investigation on phytochemical effect on cardiac remodeling appears to be promising. Nowadays, drug therapy and implantation of devices have demonstrated to ameliorate survival. Of interest, sex-gender seems to influence the response to HF canonical therapies. In fact, starting by the evidence of the feminization of world population and the scarce efficacy and safety of the traditional drugs in women, the search of alternative therapeutic tools has become mandatory. The aim of this review is to summarize the possible role of dietary phytochemicals in HF therapy and the evidence of a different sex-gender-oriented response.

Resveratrol appears to protect against oxidative stress and steroidogenesis collapse in mice fed high-calorie and high-cholesterol diet

Andrologia ◽  
2014 ◽  
Vol 47 (1) ◽  
pp. 59-65 ◽  
Author(s):  
H.-J. Wang ◽  
Q. Wang ◽  
Z.-M. Lv ◽  
C.-L. Wang ◽  
C.-P. Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Calorie

scholarly journals Antidyslipidaemic and cardioprotective effects of turmeric (Curcuma longa) in rat fed a high cholesterol diet

2020 ◽  
Vol 10 (1-s) ◽  
pp. 178-181
Author(s):  
Ikenna Kingsley Uchendu ◽  
Ifeoma Blessing Ekeigwe ◽  
Ebuka Bitrus Nnedu
Keyword(s):  
Biochemical Markers ◽  
Curcuma Longa ◽  
Density Lipoprotein ◽  
Negative Control ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Muscle Fibres ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Cardioprotective Effects

Objective: The aim of this study is to evaluate the antidyslipidaemic and cardioprotective effects of aqueous extract of Curcuma longa (AECL) in rats fed a high cholesterol diet (HCD). Methods: Twenty (20) rats were randomly grouped into four groups: A-D of five animals per group. Groups A-C received HCD (2000mg/kg, oral) and carbimazole (60mg/kg, oral) daily for eight weeks. Group A served as negative control. Group B (positive control) was treated with atorvastatin (20mg/kg), while group C served as treatment group and received AECL (400mg/kg) daily for eight weeks. Group D served as normal control and received no treatment. After the administration, biochemical markers of Lipid profiles (total cholesterol (TC), triglycerides (TG) and high density lipoprotein cholesterol (HDL-C)) were assayed using standard methods. The hearts of the rats were harvested for histopathological studies. Results: AECL significantly induced hypolipidaemia and stabilized lipid biochemical markers (p<0.05 or p<0.01); and protected the cardiac muscle fibres from injuries. Conclusion: Tumeric (Curcuma longa) has antidyslipidaemic and cardioprotective effects. Keywords: antidyslipidaemia, cardioprotection, Curcuma longa, ethnopharmacology, hypercholesterolaemia, Medicinal foods, cardiomyopathy

scholarly journals Ferroportin-Dependent Iron Homeostasis Protects against Oxidative Stress-Induced Nucleus Pulposus Cell Ferroptosis and Ameliorates Intervertebral Disc Degeneration In Vivo

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Saideng Lu ◽  
Yu Song ◽  
Rongjin Luo ◽  
Shuai Li ◽  
Gaocai Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Intervertebral Disc Degeneration ◽  
Iron Homeostasis ◽  
Nuclear Translocation ◽  
Nucleus Pulposus Cell ◽  
Intracellular Iron ◽  
Human Npcs

Ferroptosis is a specialized form of regulated cell death that is charactered by iron-dependent lethal lipid peroxidation, a process associated with multiple diseases. However, its role in the pathogenesis of intervertebral disc degeneration (IVDD) is rarely investigated. This study is aimed at investigating the role of ferroptosis in oxidative stress- (OS-) induced nucleus pulposus cell (NPC) decline and the pathogenesis of IVDD and determine the underlying regulatory mechanisms. We used tert-butyl hydroperoxide (TBHP) to simulate OS conditions around human NPCs. Flow cytometry and transmission electron microscopy were used to identify ferroptosis, while iron assay kit, Perl’s staining, and western blotting were performed to assay the intracellular iron levels. A ferroportin- (FPN-) lentivirus and FPN-siRNA were constructed and used to explore the relationship between FPN, intracellular iron homeostasis, and ferroptosis. Furthermore, hinokitiol, a bioactive compound known to specifically resist OS and restore FPN function, was evaluated for its therapeutic role in IVDD both in vitro and in vivo. The results indicated that intercellular iron overload plays an essential role in TBHP-induced ferroptosis of human NPCs. Mechanistically, FPN dysregulation is responsible for intercellular iron overload under OS. The increase in nuclear translocation of metal-regulatory transcription factor 1 (MTF1) restored the function of FPN, abolished the intercellular iron overload, and protected cells against ferroptosis. Additionally, hinokitiol enhanced the nuclear translocation of MTF1 by suppressing the JNK pathway and ameliorated the progression of IVDD in vivo. Taken together, our results demonstrate that ferroptosis and FPN dysfunction are involved in the NPC depletion and the pathogenesis of IVDD under OS. To the best of our knowledge, this is the first study to demonstrate the protective role of FPN in ferroptosis of NPCs, suggesting its potential used as a novel therapeutic target against IVDD.

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