Extracorporeal Cardiac Shock Wave-Induced Exosome Derived From Endothelial Colony-Forming Cells Carrying miR-140-3p Alleviate Cardiomyocyte Hypoxia/Reoxygenation Injury via the PTEN/PI3K/AKT Pathway

Background: Stem cell-derived exosomes have great potential in the treatment of myocardial ischemia–reperfusion injury (IRI). Extracorporeal cardiac shock waves (ECSW) as effective therapy, in part, could activate the function of exosomes. In this study, we explored the effect of ECSW-induced exosome derived from endothelial colony-forming cells on cardiomyocyte hypoxia/reoxygenation (H/R) injury and its underlying mechanisms.Methods: The exosomes were extracted and purified from the supernatant of endothelial colony-forming cells (ECFCs-exo). ECFCs-exo treated with shock wave (SW-exo) or without shock wave (CON-exo) were performed with high-throughput sequencing of the miRNA. H9c2 cells were incubated with SW-exo or CON-exo after H/R injury. The cell viability, cell apoptosis, oxidative stress level, and inflammatory factor were assessed. qRT-PCR was used to detect the expression levels of miRNA and mRNA in cells and exosomes. The PTEN/PI3K/AKT pathway-related proteins were detected by Western blotting, respectively.Results: Exosomes secreted by ECFCs could be taken up by H9c2 cells. Administration of SW-exo to H9c2 cells after H/R injury could significantly improve cell viability, inhibit cell apoptosis, and downregulate oxidative stress level (p < 0.01), with an increase in Bcl-2 protein and a decrease in Bax, cleaved caspase-3, and NF-κB protein (p < 0.05). Notably, miR-140-3p was found to be highly enriched both in ECFCs and ECFCs-exo treated with ECSW (p < 0.05) and served as a critical mediator. SW-exo increased miR-140-3p expression but decreased PTEN expression in H9c2 cells with enhanced phosphorylation of the PI3K/AKT signaling pathway. These cardioprotective effects of SW-exo on H/R injury were blunted by the miR-140-3p inhibitor. Dual-luciferase assay verified that miR-140-3p could directly target the 3′UTR of PTEN mRNA and exert a negative regulatory effect.Conclusion: This study has shown the potential of ECSW as an effective stimulation for the exosomes derived from ECFCs in vitro. SW-exo exerted a stronger therapeutic effect on H/R injury in H9c2 cells possibly via delivering exosomal miR-140-3p, which might be a novel promising strategy for the myocardial IRI.

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Development of the Express Method for Determining the Oxidative Stress Level of the Population

Food Industry ◽

10.29141/2500-1922-2018-3-4-12 ◽

2018 ◽

Vol 3 (4) ◽

Author(s):

Ekaterina V. Pastushkova ◽

Olga V. Chugunova ◽

Leonid S. Volkanin

Keyword(s):

Oxidative Stress ◽

Stress Level ◽

Express Method ◽

Oxidative Stress Level

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Evaluation of oxidative stress level: total antioxidant capacity, total oxidant status and glutathione activity in patients with Covid-19

New Microbes and New Infections ◽

10.1016/j.nmni.2021.100897 ◽

2021 ◽

pp. 100897

Author(s):

Behrouz Karkhanei ◽

Elaheh Talebi Ghane ◽

Fereshteh Mehri

Keyword(s):

Oxidative Stress ◽

Antioxidant Capacity ◽

Stress Level ◽

Total Antioxidant Capacity ◽

Total Oxidant Status ◽

Oxidative Stress Level ◽

Total Antioxidant ◽

Oxidant Status

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Ganoderic Acid A Protects Rat H9c2 Cardiomyocytes from Hypoxia-Induced Injury via Up-Regulating miR-182-5p

Cellular Physiology and Biochemistry ◽

10.1159/000495053 ◽

2018 ◽

Vol 50 (6) ◽

pp. 2086-2096 ◽

Cited By ~ 8

Author(s):

Xiaohong Zhang ◽

Can Xiao ◽

Hong Liu

Keyword(s):

Cell Viability ◽

Molecular Mechanisms ◽

Akt Pathway ◽

H9c2 Cell ◽

H9c2 Cells ◽

Ganoderic Acid ◽

Expression Levels ◽

Protein Levels ◽

Viability Loss ◽

H9c2 Cardiomyocytes

Background/Aims: Ganoderic acid A (GAA) isolated from Ganoderma lucidum, shows various benefit activities, such as anti-tumor activity, anti-HIV activity and hepatoprotective activity. However, the potential effects of GAA on hypoxia-induced injury of cardiomyocytes are still unclear. In this study, we aimed to reveal the effects of GAA on hypoxic-induced H9c2 cell injury, as well as potential underlying molecular mechanisms. Methods: Rat H9c2 cardiomyocytes were cultured in hypoxia condition with different doses of GAA. Cell viability and apoptosis were detected by CCK-8 assay and flow cytometry, respectively. qRT-PCR was performed to assess the expression levels of microRNA-182-5p (miR-182-5p) and phosphatase and tensin homologue (PTEN). Cell transfection was conducted to change the expression levels of miR-182-5p and PTEN in H9c2 cells. Finally, protein levels of key factors involved in cell proliferation, cell apoptosis and PTEN/PI3K/AKT pathway were evaluated using western blotting. Results: Hypoxia treatment significantly induced H9c2 cell viability loss and apoptosis. GAA incubation remarkably protected H9c2 cells from hypoxia-induced viability loss, proliferation inhibition and apoptosis. In addition, GAA obviously enhanced the expression level of miR-182-5p in H9c2 cells. Suppression of miR-182-5p notably alleviated the protective effects of GAA on hypoxia-treated H9c2 cells. Furthermore, miR-182-5p negatively regulated the mRNA and protein levels of PTEN in H9c2 cells. GAA attenuated hypoxia-induced inactivation of PI3K/AKT pathway in H9c2 cells by up-regulating miR-182-5p and then down-regulating PTEN. Conclusion: GAA protected rat H9c2 cardiomyocytes from hypoxia-induced injury might via up-regulating miR-182-5p, down-regulating PTEN and then activating PI3K/AKT signaling pathway.

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Influence of Baseline Oxidative Stress Level on Changes in Left Ventricle Echocardiographic Parameters in Patients with Breast Cancer Receiving Anthracycline Chemotherapy

Annals of Oncology ◽

10.1016/s0923-7534(20)34140-5 ◽

2012 ◽

Vol 23 ◽

pp. ix513

Author(s):

L. Petruzelka ◽

M. Kocik ◽

M. Zimovjanova ◽

J. Kodytkova ◽

L. Vavrova ◽

...

Keyword(s):

Breast Cancer ◽

Oxidative Stress ◽

Left Ventricle ◽

Stress Level ◽

Oxidative Stress Level ◽

Echocardiographic Parameters ◽

Anthracycline Chemotherapy

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PO-173 The Effects of Interval Exercise on oxidative stress and Smyd1-related myocardial hypertrophy in Rats with Myocardial Infarction

Exercise Biochemistry Review ◽

10.14428/ebr.v1i4.12643 ◽

2018 ◽

Vol 1 (4) ◽

Author(s):

Qiaoqin Liang ◽

Mengxin Cai ◽

Jiaqi Zhang ◽

Zhenjun Tian

Keyword(s):

Oxidative Stress ◽

Myocardial Infarction ◽

Cardiac Function ◽

Stress Level ◽

Exercise Group ◽

Control Group ◽

Coronary Artery Ligation ◽

Interval Exercise ◽

Oxidative Stress Level ◽

Sarcomere Assembly

Objective This study was carried out to investigate interval exercise on Smyd1 expression and F-actin sarcomere assembly in non-infarcted myocardium of normal and myocardial infarction(MI) rats and its possible mechanism. Methods Male SD rats were randomly divided into normal control group (C), normal interval exercise group (CE), sham-operated group (S), MI group (MI), MI with interval exercise group (ME) and MI with ROS Tempol group (MT), n=10. MI model was established by left anterior descending coronary artery ligation. Interval exercise was carried out on a small animal treadmill. MT group was given an oral solution of Tempol (2mmol/L). Hemodynamics was performed to evaluate cardiac function. HE and Masson staining were used to analyze the cross-sectional area (CSA) of cardiomyocytes and collagen volume fraction, respectively. T-SOD and MDA kits were used to detect oxidative stress. H9C2 cells were treated with H2O2. Immunofluorescence staining was used to determine Smyd1 expression and F-actin sarcomere assembly. RT-qPCR and Western blotting were used to detect the gene or protein expression of Smyd1, Trx1, Hsp90, MuRF1, cTnI, α-actinin and BNP. Results Smyd1, Trx1, Hsp90, MuRF1 and BNP expression in the peri-infarcted area were up-regulated, but cTnI and α-actinin expression and F-actin assembly were decreased. The cardiac function was reduced. Both interval exercise and Tempol intervention significantly increase the CSA and expression of Smyd1, Trx1, cTnI and α-actinin, improve the antioxidation capacity and F-actin sarcomere assembly and cardiac function, reduce the expression of Hsp90, MuRF1, BNP and ROS level, and inhibit the fibrosis of myocardium. The oxidative stress level was closely related to the Smyd1 expression. Improvement of cardiac function were correlated with Smyd1 expression. H2O2 can induce oxidative stress injuries of H9C2, and its closely related to cardiomyocytes oxidative stress level and Smyd1 expression. Conclusions Interval exercise could promote antioxidant capability and physiological cardiomyocyte hypertrophy, regulate the expression of Smyd1, Hsp90 and MuRF1 in infarcted heart; so as to improve the cardiac function. Smyd1 may participate in pathologic hypertrophy of cardiomyocytes caused by oxidative stress.

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Dapagliflozin protects H9c2 cells against injury induced by lipopolysaccharide via suppression of CX3CL1/CX3CR1 axis and NF-κB activity

Current Molecular Pharmacology ◽

10.2174/1874467214666211008142347 ◽

2021 ◽

Vol 14 ◽

Author(s):

Yousef Faridvand ◽

Maryam Nemati ◽

Elham Zamani-Gharehchamani ◽

Hamid Reza Nejabati ◽

Arezoo Rezaie Nezhad Zamani ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Viability ◽

Sglt2 Inhibitor ◽

Binding Activity ◽

Control Group ◽

H9c2 Cell ◽

H9c2 Cells ◽

Dna Binding Activity ◽

Inflammatory Conditions ◽

Tnf Α

Background: Dapagliflozin, a selective Sodium-glucose cotransporter-2 (SGLT2) inhibitor, has been shown to play a key role in the control and management of the metabolic and cardiac disease. Objective: The current study aims to address the effects of dapagliflozin on the expression of fractalkine (FKN), known as CX3CL1, and its receptors CX3CR1, Nuclear factor-kappa B(NF-κB) p65 activity, Reactive oxygen species (ROS), and inflammation in LPS-treated H9c2 cell line. Methods: H9c2 cells were cultured with lipopolysaccharide (LPS) to establish a model of LPS-induced damage and then subsequently were treated with dapagliflozin for 72 h. Our work included measurement of cell viability (MTT), Malondialdehyde (MDA), intracellular ROS, tumor necrosis factor-α (TNF-α), NF-κB activity, and expression CX3CL1/CX3CR1. Results: The results showed that LPS-induced reduction of cell viability was successfully rescued by dapagliflozin treatment. The cellular levels of MDA, ROS, and TNF-α, as an indication of cellular oxidative stress and inflammation, were significantly elevated in H9c2 cells compared to the control group. Furthermore, dapagliflozin ameliorated inflammation and oxidative stress through the modulation of the levels of MDA, TNF-α, and ROS. Correspondingly, dapagliflozin reduced the expression of CX3CL1/CX3CR1, NF-κB p65 DNA binding activity and it also attenuated nuclear acetylated NF-κB p65 in LPS-induced injury in H9c2 cells compared to untreated cells. Conclusion: These findings shed light on the novel pharmacological potential of dapagliflozin in the alleviation of LPS-induced CX3CL1/CX3CR1-mediated injury in inflammatory conditions such as sepsis-induced cardiomyopathy.

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Asprosin and Oxidative Stress Level in COVID-19 Patients

Clinical Laboratory ◽

10.7754/clin.lab.2021.210423 ◽

2022 ◽

Vol 68 (01/2022) ◽

Author(s):

E. Seyhanli ◽

Ismail Koyuncu ◽

I. Yasak ◽

H. Demir ◽

Ebru Temiz

Keyword(s):

Oxidative Stress ◽

Stress Level ◽

Oxidative Stress Level ◽

And Oxidative Stress

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Empathy and Oxidative Stress in Healthy Adults

Sustainability ◽

10.3390/su12124959 ◽

2020 ◽

Vol 12 (12) ◽

pp. 4959 ◽

Cited By ~ 1

Author(s):

Agnieszka Żelaźniewicz ◽

Judyta Nowak ◽

Agata Groyecka ◽

Piotr Sorokowski ◽

Małgorzata Dobrowolska ◽

...

Keyword(s):

Oxidative Stress ◽

Stress Level ◽

Oxidative Dna Damage ◽

Behavioral Changes ◽

Social Environments ◽

Self Assessment ◽

Adverse Conditions ◽

Oxidative Stress Level ◽

Empathy Quotient ◽

Study Participants

Empathy is crucial for normal and effective social functioning, enabling comprehension and prediction of actions in social environments. Despite its importance for maintaining social relationships in human groups, the physiological correlates of empathy are not fully known. The aim of this study was to test whether empathy is related to oxidative stress level, that may result both from internal disturbances and influence of external adverse factors. Seventy-four healthy women (Mage = 26.23, SDage = 2.88) and one hundred and one men (Mage = 28.09, SDage = 3.03) took part in the study. Participants’ empathy was evaluated with self-assessment questionnaire—Empathy Quotient (EQ). Oxidative stress level was measured with serum 8-OH-dG, a product of oxidative DNA damage. The results showed that empathy is negatively related to oxidative stress level in men but not in women, when controlled for testosterone level. Revealed sex differences may be explained by men’s greater vulnerability to various adverse conditions and harmful factors. Men, compared to women, seem to be more susceptible to behavioral changes, induced by increased oxidative stress level. The study adds to growing evidence showing that many physiological mechanisms, other than hormonal factors, that may be also related with environmental harmful factors, are related to behavioral, affective and cognitive phenomena.

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Circulating Leukocytes and Oxidative Stress in Cardiovascular Diseases: A State of the Art

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/2650429 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 3

Author(s):

Speranza Rubattu ◽

Maurizio Forte ◽

Salvatore Raffa

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Stress Level ◽

Mononuclear Cells ◽

Pathological Condition ◽

Clinical Manifestations ◽

Therapeutic Interventions ◽

Oxidative Stress Level ◽

The Impact

Increased oxidative stress from both mitochondrial and cytosolic sources contributes to the development and the progression of cardiovascular diseases (CVDs), and it is a target of therapeutic interventions. The numerous efforts made over the last decades in order to develop tools able to monitor the oxidative stress level in patients affected by CVDs rely on the need to gain information on the disease state. However, this goal has not been satisfactorily accomplished until now. Among others, the isolation of circulating leukocytes to measure their oxidant level offers a valid, noninvasive challenge that has been tested in few pathological contexts, including hypertension, atherosclerosis and its clinical manifestations, and heart failure. Since leukocytes circulate in the blood stream, it is expected that they might reflect quite closely both systemic and cardiovascular oxidative stress and provide useful information on the pathological condition. The results of the studies discussed in the present review article are promising. They highlight the importance of measuring oxidative stress level in circulating mononuclear cells in different CVDs with a consistent correlation between degree of oxidative stress and severity of CVD and of its complications. Importantly, they also point to a double role of leukocytes, both as a marker of disease condition and as a direct contributor to disease progression. Finally, they show that the oxidative stress level of leukocytes reflects the impact of therapeutic interventions. It is likely that the isolation of leukocytes and the measurement of oxidative stress, once adequately developed, may represent an eligible tool for both research and clinical purposes to monitor the role of oxidative stress on the promotion and progression of CVDs, as well as the impact of therapies.

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