scholarly journals Topical Ascorbic Acid Ameliorates Oxidative Stress-Induced Corneal Endothelial Damage via Suppression of Apoptosis and Autophagic Flux Blockage

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 943 ◽  
Author(s):  
Yi-Jen Hsueh ◽  
Yaa-Jyuhn James Meir ◽  
Lung-Kun Yeh ◽  
Tze-Kai Wang ◽  
Chieh-Cheng Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Corneal Endothelium ◽  
Cell Damage ◽  
Rabbit Model ◽  
Endothelial Damage ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Akt Phosphorylation

Compromised pumping function of the corneal endothelium, due to loss of endothelial cells, results in corneal edema and subsequent visual problems. Clinically and experimentally, oxidative stress may cause corneal endothelial decompensation after phacoemulsification. Additionally, in vitro and animal studies have demonstrated the protective effects of intraoperative infusion of ascorbic acid (AA). Here, we established a paraquat-induced cell damage model, in which paraquat induced reactive oxygen species (ROS) production and apoptosis in the B4G12 and ARPE-19 cell lines. We demonstrate that oxidative stress triggered autophagic flux blockage in corneal endothelial cells and that addition of AA ameliorated such oxidative damage. We also demonstrate the downregulation of Akt phosphorylation in response to oxidative stress. Pretreatment with ascorbic acid reduced the downregulation of Akt phosphorylation, while inhibition of the PI3K/Akt pathway attenuated the protective effects of AA. Further, we establish an in vivo rabbit model of corneal endothelial damage, in which an intracameral infusion of paraquat caused corneal opacity. Administration of AA via topical application increased its concentration in the corneal stroma and reduced oxidative stress in the corneal endothelium, thereby promoting corneal clarity. Our findings indicate a perioperative strategy of topical AA administration to prevent oxidative stress-induced damage, particularly for those with vulnerable corneal endothelia.

scholarly journals Ethanol Extract of Maclura tricuspidata Fruit Protects SH-SY5Y Neuroblastoma Cells against H2O2-Induced Oxidative Damage via Inhibiting MAPK and NF-κB Signaling

2021 ◽  
Vol 22 (13) ◽  
pp. 6946
Author(s):  
Weishun Tian ◽  
Suyoung Heo ◽  
Dae-Woon Kim ◽  
In-Shik Kim ◽  
Dongchoon Ahn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxidative Damage ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Biologically Active ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Neuroprotective Effects

Free radical generation and oxidative stress push forward an immense influence on the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Maclura tricuspidata fruit (MT) contains many biologically active substances, including compounds with antioxidant properties. The current study aimed to investigate the neuroprotective effects of MT fruit on hydrogen peroxide (H2O2)-induced neurotoxicity in SH-SY5Y cells. SH-SY5Y cells were pretreated with MT, and cell damage was induced by H2O2. First, the chemical composition and free radical scavenging properties of MT were analyzed. MT attenuated oxidative stress-induced damage in cells based on the assessment of cell viability. The H2O2-induced toxicity caused by ROS production and lactate dehydrogenase (LDH) release was ameliorated by MT pretreatment. MT also promoted an increase in the expression of genes encoding the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). MT pretreatment was associated with an increase in the expression of neuronal genes downregulated by H2O2. Mechanistically, MT dramatically suppressed H2O2-induced Bcl-2 downregulation, Bax upregulation, apoptotic factor caspase-3 activation, Mitogen-activated protein kinase (MAPK) (JNK, ERK, and p38), and Nuclear factor-κB (NF-κB) activation, thereby preventing H2O2-induced neurotoxicity. These results indicate that MT has protective effects against H2O2-induced oxidative damage in SH-SY5Y cells and can be used to prevent and protect against neurodegeneration.

scholarly journals The The Role Of Von Willenbrand Factors As The Early Detection Of Endotel Cell Damage In Youth Ages With Obesity In The Usu Medan Campus Environment

2021 ◽  
Vol 6 (1) ◽  
pp. 179-181
Author(s):  
Rusdiana ◽  
Muhammad Syahputra ◽  
Sry Suryani
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular System ◽  
Cell Damage ◽  
Single Layer ◽  
Control Group ◽  
Research Subjects ◽  
Cross Sectional ◽  
Significant Difference ◽  
Obese Subjects

Preliminary : Endothelial cells are a single layer that lines the entire vascular system. Endothelial dysfunction can be triggered by several main things, namely physical stress, oxidative stress and irritant substances. Obesity triggers an inflammatory process and metabolic disorders that will lead to increased oxidative stress. Long-term oxidative stress will cause damage to cells and tissues and trigger degenerative diseases. Damage to endothelial cells is expected to be detected by examining Von Willenbrand levels so that it can prevent complications of vascular disorders early. Method: This research is descriptive with cross sectional design. Carried out from March to October 2018 on the USU Campus. The first examination was done to measure body weight and height to determine body mass index, then performed lipid profile and blood sugar levels (KGD) in the sample, then examined von Willenbrand factor levels carried out in the integrated laboratory of USU FK using the method ELISA in both the sample group and the control group. The research subjects were adolescents aged 17-25 years with BMI> 25 kg / m2Data analysis was carried out using the T-Test statistical program, comparing two groups. Result: Of the 40 obese subjects found Von Wilenbrand level values ​​The lowest factor was 1.78 IU / ml and the highest was 35.60 IU / ml. Whereas in 40 non-obese subjects Von Wilenbrand grade values ​​were the lowest factor of 2.01 IU / ml and the highest was 45.10 IU / ml. This difference was not statistically significant (p = 0.661).Conclusion: There was no significant difference between the levels of Von Wilenbrand Factors in obese subjects with non-obese subjectsKey Words: Obesity, endothelial cells, Von Wilenbrand Factors

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

scholarly journals Treatment of corneal endothelial damage in a rabbit model with a bioengineered graft using human decellularized corneal lamina and cultured human corneal endothelium

PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0225480 ◽  
Author(s):  
Francisco Arnalich-Montiel ◽  
Adrian Moratilla ◽  
Sherezade Fuentes-Julián ◽  
Veronica Aparicio ◽  
Marta Cadenas Martin ◽  
...  
Keyword(s):  
Corneal Endothelium ◽  
Rabbit Model ◽  
Endothelial Damage ◽  
Human Corneal Endothelium

Vascular endothelium damage from catheter-induced mechanical stimulation causes catheter sleeve formation in a rabbit model

2019 ◽  
Vol 21 (3) ◽  
pp. 379-386
Author(s):  
Hidenori Tanabe ◽  
Naoto Takemura ◽  
Hisako Terao ◽  
Hitomi Hagiwara ◽  
Yasunobu Zushi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mechanical Stimulation ◽  
Vascular Endothelium ◽  
Cell Damage ◽  
Thrombus Formation ◽  
Rabbit Model ◽  
Critical Factor ◽  
External Jugular Vein ◽  
Endothelium Damage

Background: Intravenous catheters are widely used but are often removed due to complications associated with catheter sleeve formation. A catheter sleeve can develop from a thrombus, and catheter-induced vascular endothelium damage may be a critical factor for thrombus formation. We investigated the effect of catheter-induced mechanical stimulation on venous endothelial cells and catheter sleeve formation and the efficacy of anti-thrombogenic technology for preventing catheter sleeve formation in vivo. Methods: We surgically implanted poly(2-methoxyethyl acrylate)-coated and uncoated catheters with and without a stylet into the right external jugular vein of a rabbit model for 14 days. Catheter sleeve formation and the ratio of residual venous endothelial cells were compared using histological examination and immunostaining with an anti-CD31 antibody, respectively. Results: Stiffening an uncoated catheter with a stylet induced catheter sleeve formation along more than two-thirds of the length of the catheter. The ratios of residual venous endothelial cells at the tip of uncoated catheters with and without a stylet were 3% and 36%, respectively. While poly(2-methoxyethyl acrylate) coating also reduced the ratio of venous endothelial cells at the tip of the stiffened catheter (12%), it prevented external thrombus and catheter sleeve formation. Conclusion: High levels of mechanical stimulation can affect catheter-related thrombosis and promote catheter sleeve formation, and anti-thrombogenic technology such as a poly(2-methoxyethyl acrylate) coating reduces thrombus formation and can prevent catheter sleeve formation on stiffened catheters. Further studies are required to determine the maximum degree of venous endothelial cell damage before catheter sleeve formation and to compare other anti-thrombogenic technologies with poly(2-methoxyethyl acrylate) for preventing catheter sleeve formation.

Oxidative stress induced by urban fine particles in cultured EA.hy926 cells

2010 ◽  
Vol 30 (7) ◽  
pp. 579-590 ◽  
Author(s):  
Han Wei ◽  
Dan Wei ◽  
Shuo Yi ◽  
Fang Zhang ◽  
Wenjun Ding
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Fine Particles ◽  
Cell Damage ◽  
Umbilical Vein ◽  
Direct Interaction ◽  
Water Soluble ◽  
Apoptotic Pathway ◽  
Metal Elements ◽  
Ea.Hy926 Cells

It has been reported that vascular endothelia cell damage is an important precursor to the morbidity and mortality associated with cardiovascular disease exposed to airborne particulate matter (PM). The present study investigated the hypothesis that urban fine (PM2.5) particles could cause cytotoxicity via oxidative stress in human umbilical vein endothelial cells, EA.hy926. The concentrations of metal elements (Cr, Fe, Ni, Cu, Zn, Mo, Cd and Pb) in PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 were determined by inductively coupled plasma - mass spectrometry (ICP-MS). Iron (Fe), Zn and Pb were highly enriched in all the samples. Exposure of the cultured EA.hy926 cells to PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 led to cell death, reactive oxygen species (ROS) increase, mitochondrial transmembrane potential (ΔΨm) disruption and NF-κB activation, respectively. The ROS increase by exposure to PM 2.5 suspension, water-soluble and water-insoluble fractions of PM 2.5 triggered the activation of nuclear factor (NF)-κB, which means that PM2.5 particles exert cytotoxicity by an apopotic process. However, the induction of cytotoxicity by PM2.5 suspension, water-soluble and water-insoluble fractions of PM2.5 was reversed by pretreatment with superoxide dismutase (SOD). These results suggest that each fraction of PM2.5 has a potency to cause oxidative stress in endothelial cells. ROS was generated through PM2.5-mediated mitochondrial apoptotic pathway, which may induce direct interaction between metal elements and endothelia cells.

Protective effects of saffron and its active components against oxidative stress and apoptosis in endothelial cells

2018 ◽  
Vol 118 ◽  
pp. 82-89 ◽  
Author(s):  
Niloufar Rahiman ◽  
Maryam Akaberi ◽  
Amirhossein Sahebkar ◽  
Seyed Ahmad Emami ◽  
Zahra Tayarani-Najaran
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Effects ◽  
Active Components

scholarly journals Mechanisms and Treatment of Light-Induced Retinal Degeneration-Associated Inflammation: Insights from Biochemical Profiling of the Aqueous Humor

2020 ◽  
Vol 21 (3) ◽  
pp. 704 ◽  
Author(s):  
Dmitry V. Chistyakov ◽  
Viktoriia E. Baksheeva ◽  
Veronika V. Tiulina ◽  
Sergei V. Goriainov ◽  
Nadezhda V. Azbukina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinal Degeneration ◽  
Aqueous Humor ◽  
Rabbit Model ◽  
Age Related Macular Degeneration ◽  
Protective Effects ◽  
Cyclooxygenase Inhibitor ◽  
Degenerative Diseases ◽  
Age Related ◽  
Retinal Degenerative Diseases

Ocular inflammation contributes to the pathogenesis of blind-causing retinal degenerative diseases, such as age-related macular degeneration (AMD) or photic maculopathy. Here, we report on inflammatory mechanisms that are associated with retinal degeneration induced by bright visible light, which were revealed while using a rabbit model. Histologically and electrophysiologically noticeable degeneration of the retina is preceded and accompanied by oxidative stress and inflammation, as evidenced by granulocyte infiltration and edema in this tissue, as well as the upregulation of total protein, pro-inflammatory cytokines, and oxidative stress markers in aqueous humor (AH). Consistently, quantitative lipidomic studies of AH elucidated increase in the concentration of arachidonic (AA) and docosahexaenoic (DHA) acids and lyso-platelet activating factor (lyso-PAF), together with pronounced oxidative and inflammatory alterations in content of lipid mediators oxylipins. These alterations include long-term elevation of prostaglandins, which are synthesized from AA via cyclooxygenase-dependent pathways, as well as a short burst of linoleic acid derivatives that can be produced by both enzymatic and non-enzymatic free radical-dependent mechanisms. The upregulation of all oxylipins is inhibited by the premedication of the eyes while using mitochondria-targeted antioxidant SkQ1, whereas the accumulation of prostaglandins and lyso-PAF can be specifically suppressed by topical treatment with cyclooxygenase inhibitor Nepafenac. Interestingly, the most prominent antioxidant and anti-inflammatory benefits and overall retinal protective effects are achieved by simultaneous administrating of both drugs indicating their synergistic action. Taken together, these findings provide a rationale for using a combination of mitochondria-targeted antioxidant and cyclooxygenase inhibitor for the treatment of inflammatory components of retinal degenerative diseases.

scholarly journals Lipoic acid antagonizes paraquat-induced vascular endothelial dysfunction by suppressing mitochondrial reactive oxidative stress

2019 ◽  
Vol 8 (6) ◽  
pp. 918-927 ◽  
Author(s):  
Li Pang ◽  
Ping Deng ◽  
Yi-dan Liang ◽  
Jing-yu Qian ◽  
Li-Chuan Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Lipoic Acid ◽  
Microvascular Endothelial Cells ◽  
Ros Generation ◽  
Protective Effects ◽  
Migration Ability ◽  
Microvascular Endothelial

Abstract Paraquat (PQ) is a widely used herbicide in the agricultural field. The lack of an effective antidote is the significant cause of high mortality in PQ poisoning. Here, we investigate the antagonistic effects of alpha lipoic acid (α-LA), a naturally existing antioxidant, on PQ toxicity in human microvascular endothelial cells (HMEC-1). All the doses of 250, 500 and 1000 μM α-LA significantly inhibited 1000 μM PQ-induced cytotoxicity in HMEC-1 cells. α-LA pretreatment remarkably diminished the damage to cell migration ability, recovered the declined levels of the vasodilator factor nitric oxide (NO), elevated the expression level of endothelial nitric oxide synthases (eNOS), and inhibited the upregulated expression of vasoconstrictor factor endothelin-1 (ET-1). Moreover, α-LA pretreatment inhibited reactive oxygen species (ROS) generation, suppressed the damage to the mitochondrial membrane potential (ΔΨm) and mitigated the inhibition of adenosine triphosphate (ATP) production in HMEC-1 cells. These results suggested that α-LA could alleviate PQ-induced endothelial dysfunction by suppressing oxidative stress. In summary, our present study provides novel insight into the protective effects and pharmacological potential of α-LA against PQ toxicity in microvascular endothelial cells.

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