scholarly journals Platinum nanoparticles inhibit intracellular ROS generation and protect against Cold Atmospheric Plasma-induced cytotoxicity

2021 ◽  
Author(s):  
Sebnem Gunes ◽  
Zhonglei He ◽  
Renee Malone ◽  
Patrick J Cullen ◽  
James F Curtin
Keyword(s):  
Oxidative Stress ◽  
Platinum Nanoparticles ◽  
Reactive Species ◽  
Atmospheric Plasma ◽  
Hek293 Cells ◽  
Ros Generation ◽  
Protective Effects ◽  
Mitochondrial Membrane Depolarization ◽  
Cell Membrane Permeabilization ◽  
Barrier Device

AbstractPlatinum nanoparticles (PtNPs) have been investigated for their antioxidant abilities in a range of biological and other applications. The ability to reduce off-target CAP cytotoxicity would be useful in Plasma Medicine, however, little has been published to date about the ability of PtNPs to reduce or inhibit the effects of CAP. Here we investigate whether PtNPs can protect against CAP-induced cytotoxicity in cancerous and non-cancerous cell lines. PtNPs were shown to dramatically reduce intracellular reactive species (RONS) production in human U-251 MG cells. However, RONS generation was unaffected by PtNPs in medium without cells. PtNPs protect against CAP induced mitochondrial membrane depolarization, but not cell membrane permeabilization which is a CAP-induced RONS-independent event. PtNPs act as potent intracellular scavengers of reactive species and can protect both cancerous U-251 MG cells and non-cancerous HEK293 cells against CAP induced cytotoxicity. PtNPs may be useful as a catalytic antioxidant for healthy tissue and for protecting against CAP-induced tissue damage.Graphical AbstractPtNPs are potent catalase and superoxide dismutase mimetics which makes them strong antioxidant candidates for the protection of cells against oxidative stress. CAP was generated using a Dielectric Barrier Device (DBD) system with a voltage output of 75 kV at a frequency of 50 Hz. A range of concentrations of 3nm uncoated PtNPs combined with CAP were examined in human U-251 MG Glioblastoma (GBM) cells and non-cancerous human embryonic kidney HEK293 cells. The protective effects of PtNPs against CAP were explored using several biochemical indicators of oxidative stress and cytotoxicity.

scholarly journals Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Kaifeng Li ◽  
Mengen Zhai ◽  
Liqing Jiang ◽  
Fan Song ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Therapeutic Potential ◽  
Ros Generation ◽  
Protective Effects ◽  
Collagen Iii

Hyperglycemia-induced oxidative stress and fibrosis play a crucial role in the development of diabetic cardiomyopathy (DCM). Tetrahydrocurcumin (THC), a major bioactive metabolite of natural antioxidant curcumin, is reported to exert even more effective antioxidative and superior antifibrotic properties as well as anti-inflammatory and antidiabetic abilities. This study was designed to investigate the potential protective effects of THC on experimental DCM and its underlying mechanisms, pointing to the role of high glucose-induced oxidative stress and interrelated fibrosis. In STZ-induced diabetic mice, oral administration of THC (120 mg/kg/d) for 12 weeks significantly improved the cardiac function and ameliorated myocardial fibrosis and cardiac hypertrophy, accompanied by reduced reactive oxygen species (ROS) generation. Mechanically, THC administration remarkably increased the expression of the SIRT1 signaling pathway both in vitro and in vivo, further evidenced by decreased downstream molecule Ac-SOD2 and enhanced deacetylated production SOD2, which finally strengthened antioxidative stress capacity proven by repaired activities of SOD and GSH-Px and reduced MDA production. Additionally, THC treatment accomplished its antifibrotic effect by depressing the ROS-induced TGFβ1/Smad3 signaling pathway followed by reduced expression of cardiac fibrotic markers α-SMA, collagen I, and collagen III. Collectively, these finds demonstrated the therapeutic potential of THC treatment to alleviate DCM mainly by attenuating hyperglycemia-induced oxidative stress and fibrosis via activating the SIRT1 pathway.

scholarly journals Dehydroepiandrosterone Prevents H2O2-Induced BRL-3A Cell Oxidative Damage through Activation of PI3K/Akt Pathways rather than MAPK Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Longlong Li ◽  
Yao Yao ◽  
Zhihao Jiang ◽  
Jinlong Zhao ◽  
Ji Cao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Signaling Pathways ◽  
Hormone Receptors ◽  
Mapk Signaling ◽  
Ros Generation ◽  
Protective Effects ◽  
Pi3k Inhibitor Ly294002 ◽  
Beneficial Effects

Dehydroepiandrosterone (DHEA) is a popular dietary supplement that has well-known benefits in animals and humans, but there is not enough information about the mechanisms underlying its effects. The present study aimed at investigating these mechanisms through in vitro experiments on the effects of DHEA on rat liver BRL-3A cells exposed to oxidative stress through H2O2. The findings showed that DHEA increased the antioxidant enzyme activity, decreased ROS generation, and inhibited apoptosis in H2O2-treated cells. These effects of DHEA were not observed when the cells were pretreated with known antagonists of sex hormones (Trilostane, Flutamide, or Fulvestrant). Furthermore, treatment with estradiol and testosterone did not have the same protective effects as DHEA. Thus, the beneficial effects of DHEA were associated with mechanisms that were independent of steroid hormone pathways. With regard to the mechanism underlying the antiapoptotic effect of DHEA, pretreatment with DHEA was found to induce a significant decrease in the protein expression of Bax and caspase-3 and a significant increase in the protein expression of PI3K and p-Akt in H2O2-treated BRL-3A cells. These effects of DHEA were abolished when the cells were pretreated with the PI3K inhibitor LY294002. No changes were observed on the p-ERK1/2, p-p38, and p-JNK protein levels in H2O2-induced BRL-3A cells pretreated with DHEA. In conclusion, our data demonstrate that DHEA protects BRL-3A cells against H2O2-induced oxidative stress and apoptosis through mechanisms that do not involve its biotransformation into steroid hormones or the activation of sex hormone receptors. Importantly, the protective effect of DHEA on BRL-3A cells was mainly associated with PI3K/Akt signaling pathways, rather than MAPK signaling pathways.

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.

scholarly journals Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

2015 ◽  
Vol 36 (3) ◽  
pp. 966-979 ◽  
Author(s):  
Hao Liu ◽  
Ping Mao ◽  
Jia Wang ◽  
Tuo Wang ◽  
Chang-Hou Xie
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Pc12 Cells ◽  
Atp Synthesis ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Cytochrome C Release ◽  
Endogenous Antioxidant

Background: Parkinson disease (PD) is a common adult-onset neurodegenerative disorder, and PD related neuronal injury is associated with oxidative stress and mitochondrial dysfunction. Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies. Methods: The present study aimed to investigate the potential protective role of allicin in an in vitro PD model induced by 6-hydroxydopamine (6-OHDA) in PC12 cells. The protective effects were measured by cell viability, decreased lactate dehydrogenase (LDH) release and flow cytometry, and the anti-oxidative activity was determined by reactive oxygen species (ROS) generation, lipid peroxidation and the endogenous antioxidant enzyme activities. Mitochondrial function in PC12 cells was detected by mitochondrial membrane potential (MMP) collapse, cytochrome c release, mitochondrial ATP synthesis, and the mitochondrial Ca2+ buffering capacity. To investigate the potential mechanism, we also measured the expression of mitochondrial biogenesis factors, mitochondrial morphological dynamic changes, as well as detected mitochondrial dynamic proteins by western blot. Results: We found that allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure. Allicin also inhibited ROS generation, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities. These protective effects were associated with suppressed mitochondrial dysfunction, as evidenced by decreased MMP collapse and cytochrome c release, preserved mitochondrial ATP synthesis, and the promotion of mitochondrial Ca2+ buffering capacity. In addition, allicin significantly enhanced mitochondrial biogenesis and prevented fragmentation of mitochondrial network after 6-OHDA treatment. The results of western blot analysis showed that the 6-OHDA induced decrease in the expression of optic atrophy type 1 (Opa-1), increase in mitochondrial fission 1 (Fis-1) and dynamin-related protein 1 (Drp-1) were all partially revised by allicin. Conclusion: In summary, our data strongly suggested that allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.

scholarly journals Purified Sika deer antler protein attenuates GM-induced nephrotoxicity by activating Nrf2 pathway and inhibiting NF-κB pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhenyi Wang ◽  
Lulu Wang ◽  
Jing Wang ◽  
Jiacheng Luo ◽  
Haonan Ruan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Sika Deer ◽  
Kidney Injury ◽  
Annexin V ◽  
Expression Level ◽  
Hek293 Cells ◽  
Protective Effects ◽  
Deer Antler ◽  
Drug Induced

Abstract Although gentamicin is widely used as an antibiotic in clinical practice, it also has some side-effects, such as acute kidney injury, which is a common condition caused by the abuse of gentamicin. Sika deer antler protein (SDAPR) can antagonize drug-induced AKI. Since SDAPR is recognized as an effective part of velvet antler, its components were further separated. Two components named SDAP1 and SDAP2 were obtained. The protective effects of SDAPR, SDAP1 and SDAP2 on GM-induced cytotoxicity to HEK293 and its potential mechanisms were studied. MTT and xCELLigence Real-Time cell analysis showed that SDAPR, SDAP1 and SDAP2 could protect HEK293 cells from GM toxicity. Similarly, SDAPR, SDAP1 and SDAP2 can reduce ROS level, reduce oxidative stress and improve inflammation Further studies have shown that SDAPR, SDAP1 and SDAP2 upregulate the Nrf2/HO-1 pathway by increasing the expression of Nrf2 and HO-1, and down-regulate the NF-κB pathway by reducing the protein expression of NF-κB. Annexin V/PI flow cytometry and Hoechst 33258 staining showed that SDAPR, SDAP1 and SDAP2 inhibited GM-induced apoptosis in HEK293 cells. Western blot analysis showed SDAPR, SDAP1 and SDAP2 decreased expression level of Bax and Cleaved-caspase-3, and increased the expression level of Bcl-2. In addition, we examined the feasibility of SDAP1 and SDAP1 to avoid kidney injury in a GM mouse model. In conclusion, SDAPR, SDAP1 and SDAP2 can be used to prevent GM-induced HEK293 cytotoxicity, probably because they have strong anti-oxidative stress, anti-inflammatory and anti-apoptotic effects. And SDAP1 and SDAP2 can inhibit GM-induced acute kidney injury in mice.

scholarly journals Phenolic Extract from Aralia nudicaulis L. Rhizomes Inhibits Cellular Oxidative Stresses

Molecules ◽  
2021 ◽  
Vol 26 (15) ◽  
pp. 4458
Author(s):  
Quentin Lion ◽  
Andre Pichette ◽  
Mouadh Mihoub ◽  
Vakhtang Mshvildadze ◽  
Jean Legault
Keyword(s):  
Oxidative Stress ◽  
Phenolic Compounds ◽  
Defense Mechanisms ◽  
Ros Generation ◽  
Protective Effects ◽  
Growing Period ◽  
Oxidative Stresses ◽  
Biological Potential ◽  
Anti Inflammatory ◽  
Dermal Cells

UV-B and IR-A radiation are important inducers of biological changes in skin involving ROS generation. The overloading of antioxidant defense mechanisms by ROS production could lead to photoaging and photocarcinogenesis processes. Various traditional usages are reported for Aralia nudicaulis L. extracts, including treatment of dermatological disorders. Antioxidant and anti-inflammatory properties have already been reported for other Aralia species possibly due to the presence of phenolic compounds. However, the phenolic composition and the potential activity of A. nudicaulis rhizomes extract against oxidative stress and UV/IR damages have not been investigated. The main aims of this study were to prepare a fraction enriched in phenolic compounds (FEPC) from A. nudicaulis rhizomes, to identify its major phenolic compounds and to assess its potential for protective effects against oxidative stress induced by UV-B, IR-A or inflammation. A quantitative LC-MS study of FEPC shows that chlorogenic, caffeic and protocatechuic acids are the main phenolic compounds present, with concentrations of 15.6%, 15.3% and 4.8% of the total composition, respectively. With a validated analytical method, those compounds were quantified over different stages of the growing period. As for biological potential, first this extract demonstrates antioxidant and anti-inflammatory activities. Furthermore, ROS generation induced by IR-A and UV-B were strongly inhibited by A. nudicaulis extract, suggesting that Aralia nudicaulis L. rhizome extract could protect dermal cells against oxidative stress induced by UV-B and IR-A.

scholarly journals Antioxidant Activities and Protective Effects of Dendropachol, a New Bisbibenzyl Compound from Dendrobium pachyglossum, on Hydrogen Peroxide-Induced Oxidative Stress in HaCaT Keratinocytes

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 252
Author(s):  
Sakan Warinhomhoun ◽  
Chawanphat Muangnoi ◽  
Visarut Buranasudja ◽  
Wanwimon Mekboonsonglarp ◽  
Pornchai Rojsitthisak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Positive Control ◽  
Ros Generation ◽  
Protective Effects ◽  
Hacat Keratinocytes ◽  
Caspase 9 ◽  
Chemical Structures

Five compounds including a new bisbibenzyl named dendropachol (1) and four known compounds (2–5) comprising 4,5-dihydroxy-2,3-dimethoxy-9,10-dihydrophenanthrene (2), gigantol (3), moscatilin (4) and 4,5,4′-trihydroxy-3,3′-dimethoxybibenzyl (5) were isolated from a methanolic extract of Dendrobium pachyglossum (Orchidaceae). The chemical structures of the isolated compounds were characterized by spectroscopic methods. Dendropachol (1) was investigated for its protective effects on hydrogen peroxide (H2O2)-induced oxidative stress in HaCaT keratinocytes. Compound 1 showed strong free radical scavenging compared to the positive control. For the cytoprotective effect, compound 1 increased the activities of GPx and CAT and the level of GSH but reduced intracellular reactive oxygen species (ROS) generation and accumulation. In addition, compound 1 significantly diminished the expression of p53, Bax, and cytochrome C proteins, decreased the activities of caspase-3 and caspase-9, and increased Bcl-2 protein. The results suggested that compound 1 exhibited antioxidant activities and protective effects in keratinocytes against oxidative stress induced by H2O2.

scholarly journals microRNA-223-3p attenuates angiotensin II-dependent ROS effect on cell viability by targeting NLRP3 in H9c2 cells

2021 ◽  
Author(s):  
Weiran Dai ◽  
Shuang Zhou ◽  
Guoqiang Zhong ◽  
Zhiyuan Jiang
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Nlrp3 Inflammasome ◽  
Right Atrial ◽  
Luciferase Assay ◽  
Ros Generation ◽  
H9c2 Cell ◽  
Protective Effects ◽  
Ang Ii ◽  
H9c2 Cells

IntroductionRecently, enhanced activation of NLRP3 has been reported to be involved in atrial fibrillation (AF). This study aimed to detect the correlation between oxidative stress and NLRP3 and explore the role of miR-223-3p in the injury of ROS induced by Ang II.Material and methodsSerum Ang II levels were examined by ELISA kit. Fibrosis levels of right atrial appendages were determined by Masson’s staining. H9c2 cells tansfected with miR-223-3p mimics were treated with Ang II with or without MCC950 (a potent selective NLRP3 inhibitor). Cell viability was detected by CCK-8 assay. Protein abundance was detected by Western blot. MDA assay and DCFH-DA were used to measured oxidative stress. RT-qPCR was used to assay the expression of miR-223-3p and NLRP3.ResultsTotally, 43 patients enrolled in this study, including 20 patients with persistent (chronic) AF (cAF). Comparing with sinus rhythm (SR) group, we found an enhanced activation of NLRP3 inflammasome which were positively correlated with oxidative stress and serum Ang II level in cAF patients. Ang II induced ROS generation and inhibited the H9c2 cell viability. In addition, overexpression of miR-223-3p functioned as MCC950 which inhibited the expression of NLRP3 inflammasome and partly attenuated the effects of ROS induced by Ang II on H9c2 cell viability. Lastly, we used luciferase assay to confirm NLRP3 as a direct target gene of miR-223-3p.ConclusionsmiR-223-3p has protective effects on oxidative stress induced by Ang II in AF by targeting NLRP3 and could provide a new potential intervention targets for treatment of AF.

scholarly journals Neuroprotective Effects of Glochidion zeylanicum Leaf Extract against H2O2/Glutamate-Induced Toxicity in Cultured Neuronal Cells and Aβ-Induced Toxicity in Caenorhabditis elegans

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 800
Author(s):  
Chatrawee Duangjan ◽  
Panthakarn Rangsinth ◽  
Shaoxiong Zhang ◽  
Xiaojie Gu ◽  
Michael Wink ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Leaf Extract ◽  
Neuronal Cells ◽  
Antioxidant Properties ◽  
Ros Generation ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Antioxidant Genes ◽  
Age Related

Oxidative stress plays a crucial role in the development of age-related neurodegenerative diseases. Previously, Glochidion zeylanicum methanol (GZM) extract has been reported to have antioxidant and anti-aging properties. However, the effect of GZM on neuroprotection has not been reported yet; furthermore, the mechanism involved in its antioxidant properties remains unresolved. The study is aimed to demonstrate the neuroprotective properties of GZM extract and their underlying mechanisms in cultured neuronal (HT-22 and Neuro-2a) cells and Caenorhabditis elegans models. GZM extract exhibited protective effects against glutamate/H2O2-induced toxicity in cultured neuronal cells by suppressing the intracellular reactive oxygen species (ROS) generation and enhancing the expression of endogenous antioxidant enzymes (SODs, GPx, and GSTs). GZM extract also triggered the expression of SIRT1/Nrf2 proteins and mRNA transcription of antioxidant genes (NQO1, GCLM, and EAAT3) which are the master regulators of cellular defense against oxidative stress. Additionally, GZM extract exhibited protective effects to counteract β-amyloid (Aβ)-induced toxicity in C. elegans and promoted neuritogenesis properties in Neuro-2a cells. Our observations suggest that GZM leaf extract has interesting neuritogenesis and neuroprotective potential and can possibly act as potential contender for the treatment of oxidative stress-induced Alzheimer’s disease (AD) and related neurodegenerative conditions; however, this needs to be studied further in other in vivo systems.

scholarly journals AstragalusPolysaccharide Suppresses Doxorubicin-Induced Cardiotoxicity by Regulating the PI3k/Akt and p38MAPK Pathways

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Yuan Cao ◽  
Yang Ruan ◽  
Tao Shen ◽  
Xiuqing Huang ◽  
Meng Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Neonatal Rat ◽  
Ros Generation ◽  
Signal Pathways ◽  
Mouse Heart ◽  
Protective Effects ◽  
Injury Model ◽  
Underlying Mechanisms ◽  
Heart Failure Model

Background. Doxorubicin, a potent chemotherapeutic agent, is associated with acute and chronic cardiotoxicity, which is cumulatively dose-dependent.Astragaluspolysaccharide (APS), the extract ofAstragalus membranaceuswith strong antitumor and antiglomerulonephritis activity, can effectively alleviate inflammation. However, whether APS could ameliorate chemotherapy-induced cardiotoxicity is not understood. Here, we investigated the protective effects of APS on doxorubicin-induced cardiotoxicity and elucidated the underlying mechanisms of the protective effects of APS.Methods. We analyzed myocardial injury in cancer patients who underwent doxorubicin chemotherapy and generated a doxorubicin-induced neonatal rat cardiomyocyte injury model and a mouse heart failure model. Echocardiography, reactive oxygen species (ROS) production, TUNEL, DNA laddering, and Western blotting were performed to observe cell survival, oxidative stress, and inflammatory signal pathways in cardiomyocytes.Results. Treatment of patients with the chemotherapeutic drug doxorubicin led to heart dysfunction. Doxorubicin reduced cardiomyocyte viability and induced C57BL/6J mouse heart failure with concurrent elevated ROS generation and apoptosis, which, however, was attenuated by APS treatment. In addition, there was profound inhibition of p38MAPK and activation of Akt after APS treatment.Conclusions. These results demonstrate that APS could suppress oxidative stress and apoptosis, ameliorating doxorubicin-mediated cardiotoxicity by regulating the PI3k/Akt and p38MAPK pathways.

Sign in / Sign up

Export Citation Format

Share Document