scholarly journals Synergistic Protective Effect of Curcumin and Resveratrol against Oxidative Stress in Endothelial EAhy926 Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xian Zhou ◽  
Sualiha Afzal ◽  
Yan-Fang Zheng ◽  
Gerald Münch ◽  
Chun Guang Li
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Caspase 3 ◽  
Combination Index ◽  
New Combination ◽  
Ros Production ◽  
Protective Effects ◽  
Sod Activity ◽  
Index Model ◽  
Induced Changes

Curcumin (C) and resveratrol (R) are two well-known nutraceuticals with strong antioxidant activity that can protect cells from oxidative stress. This study aims to investigate the synergy of CR combinations in protecting human endothelial EAhy926 cells against H2O2-induced oxidative stress and its related mechanisms. C and R as individual compounds as well as CR combinations at different ratios were screened for their protective effects against H2O2 (2.5 mM) induced cell death assessed by cell viability assays. The synergistic interaction was analysed using the combination index model. The effects of optimal CR combinations on caspase-3 activity, ROS level, SOD activity, NAD cellular production, expression of Nrf2 and HO-1, and Nrf2 translocation were determined. CR combinations produced a synergistic protection against that of H2O2-induced changes in cell viability, caspase-3 activity, and ROS production. The strongest effect was observed for CR with the ratio of 8 : 2. Further experiments showed that CR 8 : 2 exhibited significantly greater effects in increasing Nrf2 translocation and expressions of Nrf2 and HO-1 proteins, as well as SOD activity and total cellular NAD production, than that of C or R alone. The findings demonstrate that combination of C and R produced a strong synergy in activity against H2O2-induced oxidative stress in EAhy926 cells. The mechanism of this synergy involves the activation of Nrf2-HO-1 signaling pathway and promotion of antioxidant enzymes. Further studies on CR synergy may help develop a new combination therapy for endothelial dysfunction and other conditions related to oxidative stress.

scholarly journals Effects of oral and intraperitoneal magnesium treatment against cadmium-induced oxidative stress in plasma of rats

2012 ◽  
Vol 63 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Aleksandra Buha ◽  
Zorica Bulat ◽  
Danijela Đukić-Ćosić ◽  
Vesna Matović
Keyword(s):  
Oxidative Stress ◽  
Rat Plasma ◽  
Control Group ◽  
Protective Agent ◽  
Protective Effects ◽  
Negative Effects ◽  
Sod Activity ◽  
Total Oxidative Status ◽  
Intraperitoneal Treatment ◽  
Induced Changes

Cadmium (Cd) has been recognised as one of the most important environmental and industrial pollutants, and up-to-date investigations have shown that one of the mechanisms of its toxicity is associated with the induction of oxidative stress. The aim of this study was to determine the connection between acute oral and intraperitoneal exposure to Cd and parameters indicative of oxidative stress in the plasma of rats, as well as to examine the potential protective effect of magnesium (Mg) in conditions of acute oral and intraperitoneal Cd poisoning. The experiment was performed on male albino Wistar rats (n=40) randomly divided into control group, Cdor group that received 30 mg kg-1 b.w. Cd by oral gavage, Cd+Mgor group that orally received 50 mg kg-1 b.w. Mg one hour before oral Cd, Cdip group that received 1.5 mg kg-1 b.w. Cd intraperitoneally, and Cd+Mgip group that intraperitoneally received 3 mg kg-1 b.w. Mg 10 min before intraperitoneal Cd. The animals were sacrifi ced 24 h after treatment and the following parameters were measured: superoxidedismutase activity, superoxide anion, total oxidative status, advanced oxidation protein products, and malondialdehyde. All parameters of oxidative stress in rat plasma were negatively affected by Cd treatment with more pronounced negative effects after intraperitoneal treatment, with the exception of superoxide dismutase (SOD) activity. Although both oral and intraperitoneal Mg pretreatment had protective effects, more pronounced benefi cial effects were observed after oral administration, since it managed to completely prevent Cd-induced changes in the investigated parameters. The observed results support the use of Mg as potential protective agent against toxic effects caused by Cd.

scholarly journals DIHYDROMYRICETIN ATTENUATES HIGH GLUCOSE-INDUCED CASPASE 3 EXPRESSION, ROS PRODUCTION AND INCREASES AMPK PHOSPHONYLATION IN PC12 CELLS

2019 ◽  
Vol 8 (5) ◽  
Author(s):  
Shuo Wang ◽  
Lin Wang ◽  
Haijian Li ◽  
Shumei Wang ◽  
Zhenzhen Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Caspase 3 ◽  
Cell Damage ◽  
Neural Function ◽  
Ros Production ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Central Nervous System Dysfunction ◽  
Amp Activated Protein Kinase

Dihydromyricetin (DMY) has a protective effect on neural function under central nervous system dysfunction conditions. There is growing interest concerning the beneficial effects of DMY on treating diabetic neuropathy (DN). This study was carried to detect protective effects of DMY on high glucose (HG)-induced cell damage and related mechanisms. The effect of DMY on cell survival was detected by MTT assay. Caspase-3 and phosphorylated AMP-activated protein kinase (AMPK) was evaluated by Western blotting. The effects of DMY and AMPK agonist AICAR on ROS production was determined. Our results showed that DMY treatment protect against HG-induced cell damage. DMY treatment significantly reduced the expression of caspase-3 and phosphorylated AMPK. ROS production was inhibited by DMY or AMPK agonist AICAR treatment. These studies demonstrate that DMY may inhibit ROS production, caspase-3 expression through AMPK pathway. Keywords: dihydromyricetin, caspase, oxidative stress

Effect of Donepezil on Vascular Dementia in Rats via PI3K/AKT Pathway

2022 ◽  
Vol 12 (5) ◽  
pp. 1046-1052
Author(s):  
Jianmin Zhang ◽  
Qianwen Zhu ◽  
Xingnan Wang ◽  
Jian Wang
Keyword(s):  
Oxidative Stress ◽  
Vascular Dementia ◽  
Learning And Memory ◽  
Brain Tissue ◽  
Caspase 3 ◽  
Akt Pathway ◽  
Ros Production ◽  
Sod Activity ◽  
Ht22 Cells ◽  
Stress Injury

Background: Previous studies have shown that Donepezil has therapeutic effects on vascular dementia (VD). PI3K/AKT involves in oxidative stress injury and cell apoptosis. This study investigated whether Donepezil affects the neurological function and apoptosis of VD mice via PI3K/AKT signaling. Methods: Mice were assigned into Sham group, VD group, VD+Donepezil groupfollowed by analysis of mice learning and memory ability by Water maze test, p-AKT expression by Western blot, Caspase-3 activity, MDA content, SOD activity and GSH-Px in hippocampus. HT22 cells were cultured and separated into control group, I-R group and I-R+Donepezil group followed by measuring p-AKT level, ROS content and apoptosis. Results: Learning and memory abilities of VD group mice were significantly decreased, Caspase-3 activity and MDA in brain tissue were significantly increased, along with decreased SOD activity, GSH-Px and p-AKT level. Donepezil treatment can significantly improve VD mice learning and memory ability, reduce Caspase-3 activity and MDA in brain tissue, increase SOD activity, GSH-Px and p-AKT level. In vitro, I-R treatment significantly induced apoptosis of HT22 cells, increased ROS production and decreased p-AKT level. Donepezil treatment could up-regulate p-AKT in HT22 cells and reduce apoptosis and ROS production in HT22 cells. Conclusion: Donepezil improves the function of brain nerve in VD mice through regulating PI3K/AKT pathway, thus reducing oxidative stress injury and apoptosis of brain nerve cells.

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134

2021 ◽  
pp. 096032712110237
Author(s):  
Y-J Li ◽  
D-Z Zhang ◽  
Y Xi ◽  
C-A Wu
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Damage ◽  
Annexin V ◽  
Protective Effects ◽  
Gene And Protein Expression ◽  
And Oxidative Stress

Objective: To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells. Methods: Hydrogen peroxide (H2O2)-stimulated PC12 cells were divided into control, H2O2, DEX + H2O2, miR-NC/inhibitor + H2O2, and miR-NC/ mimic + DEX + H2O2 groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit. Results: DEX treatment decreased H2O2-elevated miR-134 expression. H2O2-induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H2O2-induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H2O2-induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic. Conclusion: DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H2O2-induced PC12 cells by inhibiting the expression of miR-134.

scholarly journals Antiepileptic Effects of Protein-Rich Extract from Bombyx batryticatus on Mice and Its Protective Effects against H2O2-Induced Oxidative Damage in PC12 Cells via Regulating PI3K/Akt Signaling Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Meibian Hu ◽  
Yujie Liu ◽  
Liying He ◽  
Xing Yuan ◽  
Wei Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Maximal Electroshock ◽  
Protective Effects ◽  
Caspase 9 ◽  
Protein Rich

Bombyx batryticatus is a known traditional Chinese medicine (TCM) utilized to treat convulsions, epilepsy, cough, asthma, headaches, and purpura in China for thousands of years. This study is aimed at investigating the antiepileptic effects of protein-rich extracts from Bombyx batryticatus (BBPs) on seizure in mice and exploring the protective effects of BBPs against H2O2-induced oxidative stress in PC12 cells and their underlying mechanisms. Maximal electroshock-induced seizure (MES) and pentylenetetrazole- (PTZ-) induced seizure in mice and the histological analysis were carried out to evaluate the antiepileptic effects of BBPs. The cell viability of PC12 cells stimulated by H2O2 was determined by MTT assay. The apoptosis and ROS levels of H2O2-stimulated PC12 cells were determined by flow cytometry analysis. Furthermore, the levels of malondialdehyde (MDA), superoxide dismutase (SOD), lactate dehydrogenase (LDH), and glutathione (GSH) in PC12 cells were assayed by ELISA and expressions of caspase-3, caspase-9, Bax, Bcl-2, PI3K, Akt, and p-Akt were evaluated by Western blotting and quantitative real-time polymerase chain reaction (RT-qPCR) assays. The results revealed that BBPs exerted significant antiepileptic effects on mice. In addition, BBPs increased the cell viability of H2O2-stimulated PC12 cells and reduced apoptotic cells and ROS levels in H2O2-stimulated PC12 cells. By BBPs treatments, the levels of MDA and LDH were reduced and the levels of SOD and GSH-Px were increased in H2O2-stimulated PC12 cells. Moreover, BBPs upregulated the expressions of PI3K, Akt, p-Akt, and Bcl-2, whereas they downregulated the expressions of caspase-9, caspase-3, and Bax in H2O2-stimulated PC12 cells. These findings suggested that BBPs possessed potential antiepileptic effects on MES and PTZ-induced seizure in mice and protective effects on H2O2-induced oxidative stress in PC12 cells by exerting antioxidative and antiapoptotic effects via PI3K/Akt signaling pathways.

Oxidative stress and genotoxicity of co-exposure to chlorpyrifos and aflatoxin B1 in HepG2 cells

2020 ◽  
Vol 36 (5) ◽  
pp. 336-345
Author(s):  
Anupon Tadee ◽  
Pramote Mahakunakorn ◽  
Supatra Porasuphatana
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Paraoxonase 1 ◽  
Hepatic Tissue ◽  
Ros Production ◽  
Combined Exposure ◽  
Sod Activity ◽  
Index Value ◽  
Aflatoxin B

Chlorpyrifos (CPF) and aflatoxin B1 (AFB1) are each known to adversely affect hepatic tissue individually, but their combined hepatic effects have never been previously investigated. HepG2 cell viability, oxidative status, and genetic impairment were examined after exposing HepG2 cells to: (1) CPF alone, (2) AFB1 alone, and (3) CPF and AFB1 combined (20:1). CPF exposure decreased cell viability, reduced glutathione (GSH) content, and superoxide dismutase (SOD) activity but increased both glutathione peroxidase (GPx) and paraoxonase 1 activity. AFB1 exposure decreased cell viability and GSH content but increased reactive oxygen species (ROS) production. CPF and AFB1 combined exposure decreased GSH content ( p < 0.05) further over individual CPF and AFB1 exposures. Induction of micronucleus formation was detected in AFB1-treated cells but undetected in both CPF and combination-treated cells. In conclusion, cytotoxic effects caused by combined exposure were antagonistic, as shown by a combination index value of 1.67. Although no change in ROS production was observed in CPF groups, the overall results confirmed the occurrence of oxidative stress through the alterations of GSH content, GPx, and SOD activity. Only intracellular GSH was evidently changed upon exposure to CPF and AFB1 combined. Thus, this study suggested cellular GSH as a potential indicator for detecting the combined effects of CPF and AFB1 in HepG2 cells, the detection of which could be adapted to estimate the potential toxicity of additional multiple toxicant exposures.

Epigallocatechin Gallate Protects against TNFα- or H2O2- Induced Apoptosis by Modulating Iron Related Proteins in a Cell Culture Model

2018 ◽  
Vol 88 (3-4) ◽  
pp. 158-165 ◽  
Author(s):  
Qi Xu ◽  
Anumantha G. Kanthasamy ◽  
Manju B. Reddy
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Caspase 3 ◽  
Epigallocatechin Gallate ◽  
Ros Generation ◽  
Dependent Manner ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Cell Viability Assay ◽  
Hepcidin Expression

Abstract. Oxidative stress, iron dysregulation, and inflammation have been implicated in the pathogenesis of Parkinson’s disease (PD). Considering the entwined relationship among these factors, epigallocatechin gallate (EGCG) may be a good candidate for PD treatment due to its protective effects against those factors. The objective of this study is to determine whether EGCG protects N27 dopaminergic neuronal cells from H2O2 - and TNFα- induced neurotoxicity. Seven treatments were included: control, H2O2, TNFα, FeSO4, H2O2 + EGCG, TNFα + EGCG, FeSO4 + EGCG. Cells were pretreated with 10 μM EGCG, followed by 50 μM H2O2, 30 ng/ml TNFα or 50 μM FeSO4. Neuroprotective effects of EGCG were assessed by cell viability assay, caspase-3 activity, intracellular reactive oxygen species (ROS) generation, and iron related protein expressions. Caspase-3 activity was increased to 2.8 fold (P < 0.001) and 1.5 fold (P < 0.01) with H2O2 and TNFα treatment; However, EGCG pretreatment significantly decreased the caspase activity by 50.2% (P < 0.001) and 30.1% (P < 0.05). Similarly, cell viability was reduced to 69.2% (P < 0.01) and 89% (P < 0.01) by H2O2 and TNFα, which was partially blocked by EGCG pretreatment. Also, EGCG significantly (P < 0.001) protected against H2O2- induced ROS in a time dependent manner. In addition, both H2O2 and TNFα significantly (P < 0.05) upregulated hepcidin expression and marginally reduced ferroportin (Fpn) expression unlike iron treatment alone. Collectively, our results show that EGCG protects against both TNFα- and H2O2- induced neuronal apoptosis. The observed neuroprotection may be through the inhibition of oxidative stress and inflammation which is possibly mediated mainly by hepcidin and partially by Fpn.

Hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in HepG2 cells

2020 ◽  
Vol 01 ◽  
Author(s):  
Ayşe Mine Yılmaz ◽  
Gökhan Biçim ◽  
Kübra Toprak ◽  
Betül Karademir Yılmaz ◽  
Irina Milisav ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Hydrogen Peroxide ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Proteasome Activity ◽  
Cell Cycle Phases ◽  
Induced Changes ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

Protective Effects of Ginsenosides on 17α-Ethynyelstradiol-Induced Intrahepatic Cholestasis via Anti-Oxidative and Anti-Inflammatory Mechanisms in Rats

2017 ◽  
Vol 45 (08) ◽  
pp. 1613-1629 ◽  
Author(s):  
Yan-Jiao Xu ◽  
Zao-Qin Yu ◽  
Cheng-Liang Zhang ◽  
Xi-Ping Li ◽  
Cheng-Yang Feng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alkaline Phosphatase ◽  
Superoxide Dismutase ◽  
Protein Expression ◽  
Intrahepatic Cholestasis ◽  
Serum Levels ◽  
Total Bile Acid ◽  
Protective Effects ◽  
Sod Activity ◽  
Mda Content

The present study was designed to assess the effects and potential mechanisms of ginsenosides on 17[Formula: see text]-ethynyelstradiol (EE)-induced intrahepatic cholestasis (IC). Ginsenoside at doses of 30, 100, 300[Formula: see text]mg/kg body weight was intragastrically (i.g.) given to rats for 5 days to examine the effect on EE-induced IC. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bile acid (TBA) were measured. Hepatic malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. Protein expression of proinflammatory cytokines TNF-[Formula: see text], IL-6 and IL-1[Formula: see text] was analyzed by immunohistochemistry and Western blot. Results indicated that ginsenosides remarkably prevented EE-induced increase in the serum levels of AST, ALT, ALP and TBA. Moreover, the elevation of hepatic MDA content induced by EE was significantly reduced, while hepatic SOD activities were significantly increased when treated with ginsenosides. Histopathology of the liver tissue showed that pathological injuries were relieved after treatment with ginsenosides. In addition, treatment with ginsenosides could significantly downregulate the protein expression of TNF-[Formula: see text], IL-6 and IL-1[Formula: see text] compared with EE group. These findings indicate that ginsenosides exert the hepatoprotective effect on EE-induced intrahepatic cholestasis in rats, and this protection might be attributed to the attenuation of oxidative stress and inflammation.

scholarly journals To Evaluate the Effect of Vitamin E Therapy on the Oxidative Stress Markers (Nitric Oxide, SOD, Glutathione Peroxidase) & Vitamin E Levels in Pulmonary Tuberculosis Patients

2020 ◽  
Vol 9 (40) ◽  
pp. 2970-2975
Author(s):  
Rohit John Chaudhary ◽  
Bharti Kwatra Uppal
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Pulmonary Tuberculosis ◽  
Older Age ◽  
Control Group ◽  
Ros Production ◽  
Age Group ◽  
Sod Activity

BACKGROUND Severe oxidative stress has been reported in TB patients because of infection associated with malnutrition and poor immunity. Mycobacteria can induce reactive oxygen species (ROS) production by activating phagocytes, and enhanced ROS production may promote tissue injury and inflammation. We wanted to compare the effect of antioxidant administration in the outcome of ATT treatment between the test and the control group. METHODS This perspective study was conducted in the Departments of Biochemistry and Chest Medicine, CMC & Hospital. Hundred patients (fifty controls and fifty tests) who were diagnosed as pulmonary tuberculosis and started on DOT therapy under RNTCP during this period were included in the study. Each participant in the study was subjected to the following test at the first visit, 2nd month and 6th month follow up (biochemical markers Nitric oxide, SOD, Glutathione Peroxidase and Vitamin E levels). Statistical analysis was done using SPSS version. RESULTS The results were based on four categories (male / female, alcoholic / non-alcoholic, smoker / non-smoker, and younger / older age group). Females had responded better with greater fall in percentage of nitric oxide values (69 %) than males (64.1 %). The mean of SOD activity (277.5 + / - 31.5) was more in smokers than non-smokers (261.3 + / - 36.0) & percentage fall of nitric oxide in smokers (65 %) & non-smokers (67 %). In alcoholics the percentage fall of nitric oxide (68.3 %) was higher with more SOD activity (Mean 278.7 + / - 27.6) than non-alcoholics (Mean 256 + / - 38.0) indicating a positive correlation of smoking & alcoholism with tuberculosis. Younger age group responded better with more fall in the percentage of nitric oxide (67 %) & mean SOD activity (265.8 + / - 30.1) than older age group. CONCLUSIONS Antioxidant supplementation reduces oxidative stress, improves the effectiveness of ATT therapy, and thus helps in improving the outcome in pulmonary tuberculosis. KEY WORDS Pulmonary TB, ATT (Anti-Tubercular Treatment), Antioxidants & Free Radicals

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