scholarly journals Antioxidant and Wound Healing Property of Gelsolin in 3T3-L1 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Bhavna Vaid ◽  
Bhupinder Singh Chopra ◽  
Sachin Raut ◽  
Amin Sagar ◽  
Maulik D. Badmalia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Plasma Gelsolin ◽  
Total Antioxidant ◽  
Effective Role ◽  
Healing Property ◽  
Injury Recovery

Delineation of factors which affect wound healing would be of immense value to enable on-time or early healing and reduce comorbidities associated with infections or biochemical stress like diabetes. Plasma gelsolin has been identified earlier to significantly enable injury recovery compared to placebo. This study evaluates the role of rhuGSN for its antioxidant and wound healing properties in murine fibroblasts (3T3-L1 cell line). Total antioxidant capacity of rhuGSN increased in a concentration-dependent manner (0.75-200 μg/mL). Cells pretreated with 0.375 and 0.75 μg/mL rhuGSN for 24 h exhibited a significant increase in viability in a MTT assay. Preincubation of cells with rhuGSN for 24 h followed by oxidative stress induced by exposure to H2O2 for 3 h showed cytoprotective effect. rhuGSN at 12.5 and 25 μg/mL concentration showed an enhanced cell migration after 20 h of injury in a scratch wound healing assay. The proinflammatory cytokine IL-6 levels were elevated in the culture supernatant. These results establish an effective role of rhuGSN against oxidative stress induced by H2O2 and in wound healing of 3T3-L1 fibroblast cells.

scholarly journals EVALUATION OF THE PROTECTIVE EFFECT OF GALLIC ACID AGAINST ARSENIC-INDUCED GENOTOXICITY IN HEPG2 CELL LINE

2020 ◽  
pp. 98-103
Author(s):  
NIDHYA TERESA JOSEPH ◽  
RAJASEKHAR MOKA
Keyword(s):  
Oxidative Stress ◽  
Gallic Acid ◽  
Mutagenic Effect ◽  
Time Dependent ◽  
Dependent Manner ◽  
Cellular Viability ◽  
Concentration Dependent Manner ◽  
Low Concentrations ◽  
Ameliorative Effect

Objective: Arsenic has cytotoxic as well as mutagenic effect in human health due to its indirect effect on oxidative stress on the cells. We aimed to find out the effect of gallic acid (GA), a well-known natural antioxidant in ameliorating in heavy metal toxicity. Methods: MTT assay was performed to determine the cytotoxicity of sodium arsenite (NaAsO2) on HepG2 cells with the cytoprotectant GA at varying concentrations for exposure durations of 6 h, 12 h, and 24 h. Similarly, the alkaline version of the comet assay was performed to investigate the genotoxicity and assessment of oxidative stress of the cells using flow cytometry. Results: Cells treated with NaAsO2 at various doses spanning a broad range of concentrations (5–500 μM) showed a dose- and time-dependent decrease in cellular viability as observed. However, the effect of the proposed protectant, GA showed an increase in cellular viability in a concentration-dependent manner. Conclusion: We assessed the cytotoxicity and genotoxicity induced by NaAsO2 to provide insight into the role of GA on arsenic-induced toxicity in liver cells and to shed light on its possible ameliorative effect at low concentrations in a time-dependent manner.

scholarly journals Exposure top,p′-DDE Induces Morphological Changes and Activation of the PKCα-p38-C/EBPβPathway in Human Promyelocytic HL-60 Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Nallely A. Torres-Avilés ◽  
Damaris Albores-García ◽  
Ana L. Luna ◽  
Monica Moreno-Galván ◽  
Mariana Salgado-Bustamante ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Morphological Changes ◽  
Myeloid Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Protein Levels ◽  
Immature Myeloid Cells ◽  
Bone Marrow Disorders

Dichlorodiphenyldichloroethylene (p,p′-DDE), the most persistent metabolite of dichlorodiphenyltrichloroethane (DDT), is still present in the human population. Both are present in the bone marrow of patients with bone marrow disorders, but thus far there are no studies that assess the capability ofp,p′-DDE to affect myeloid cells. The aim of this study was to determine the effect ofp,p′-DDE on promyelocytic cell differentiation and intracellular pathways related to this event.p,p′-DDE induced morphological changes compatible with promyelocytic differentiation in a concentration-dependent manner. Thep,p′-DDE effect onCa2+i, C/EBPβprotein levels, PKCαand p38 activation, and the role of oxidative stress or PLA2 was assayed. Exposure to 1.9 μg/mL ofp,p′-DDE increasedCa2+i, PKCα, p38, and C/EBPβprotein levels; the increase of nuclear C/EBPβprotein was dependent on p38. PKCαphosphorylation was dependent on PLA2 andp,p′-DDE-induced oxidative stress. p38 phosphorylation induced byp,p′-DDE was dependent on PLA2, PKC activation, and oxidative stress. These effects ofp,p′-DDE at concentrations found in human bone marrow may induce alterations in immature myeloid cells and could affect their cellular homeostasis. In order to establish the risk from exposure top,p′-DDE on the development of bone marrow disorders in humans, these effects deserve further study.

scholarly journals NF-κB and FosB mediate inflammation and oxidative stress in the blast lung injury of rats exposed to shock waves

2021 ◽  
Author(s):  
Hong Wang ◽  
Wenjuan Zhang ◽  
Jinren Liu ◽  
Junhong Gao ◽  
Le Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Shock Waves ◽  
Time Dependent ◽  
Inflammatory Factors ◽  
Control Group ◽  
Dependent Manner ◽  
Total Antioxidant ◽  
Blast Lung Injury ◽  
And Oxidative Stress

Abstract Blast lung injury (BLI) is the major cause of death in explosion-derived shock waves; however, the mechanisms of BLI are not well understood. To identify the time-dependent manner of BLI, a model of lung injury of rats induced by shock waves was established by a fuel air explosive. The model was evaluated by hematoxylin and eosin staining and pathological score. The inflammation and oxidative stress of lung injury were also investigated. The pathological scores of rats’ lung injury at 2 h, 24 h, 3 days, and 7 days post-blast were 9.75±2.96, 13.00±1.85, 8.50±1.51, and 4.00±1.41, respectively, which were significantly increased compared with those in the control group (1.13±0.64; P<0.05). The respiratory frequency and pause were increased significantly, while minute expiratory volume, inspiratory time, and inspiratory peak flow rate were decreased in a time-dependent manner at 2 and 24 h post-blast compared with those in the control group. In addition, the expressions of inflammatory factors such as interleukin (IL)-6, IL-8, FosB, and NF-κB were increased significantly at 2 h and peaked at 24 h, which gradually decreased after 3 days and returned to normal in 2 weeks. The levels of total antioxidant capacity, total superoxide dismutase, and glutathione peroxidase were significantly decreased 24 h after the shock wave blast. Conversely, the malondialdehyde level reached the peak at 24 h. These results indicated that inflammatory and oxidative stress induced by shock waves changed significantly in a time-dependent manner, which may be the important factors and novel therapeutic targets for the treatment of BLI.

Inducible nitric oxide synthase augments injury elicited by oxidative stress in rat cardiac myocytes

1998 ◽  
Vol 274 (1) ◽  
pp. C245-C252 ◽  
Author(s):  
Junsuke Igarashi ◽  
Masashi Nishida ◽  
Shiro Hoshida ◽  
Nobushige Yamashita ◽  
Hiroaki Kosaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Myocardial Injury ◽  
No Production ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
No Donor ◽  
Oxide Synthase ◽  
Gpx Activity

The effects of nitric oxide (NO) produced by cardiac inducible NO synthase (iNOS) on myocardial injury after oxidative stress were examined. Interleukin-1β induced cultured rat neonatal cardiac myocytes to express iNOS. After induction of iNOS,l-arginine enhanced NO production in a concentration-dependent manner. Glutathione peroxidase (GPX) activity in myocytes was attenuated by elevated iNOS activity and by an NO donor, S-nitroso- N-acetyl-penicillamine (SNAP). Although NO production by iNOS did not induce myocardial injury, NO augmented release of lactate dehydrogenase from myocyte cultures after addition of H2O2(0.1 mM, 1 h). Inhibition of iNOS with Nω-nitro-l-arginine methyl ester ameliorated the effects of NO-enhancing treatments on myocardial injury and GPX activity. SNAP augmented the myocardial injury induced by H2O2. Inhibition of GPX activity with antisense oligodeoxyribonucleotide for GPX mRNA increased myocardial injury by H2O2. Results suggest that the induction of cardiac iNOS promotes myocardial injury due to oxidative stress via inactivation of the intrinsic antioxidant enzyme, GPX.

The P-element-induced silencing effect of KP transposons is dose dependent in Drosophila melanogaster

Genome ◽  
2011 ◽  
Vol 54 (9) ◽  
pp. 752-762 ◽  
Author(s):  
Alireza Sameny ◽  
John Locke
Keyword(s):  
Drosophila Melanogaster ◽  
Critical Role ◽  
Mutagenic Effect ◽  
P Element ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
P Elements ◽  
Single Well ◽  
Dose Dependent

Transposable elements are found in the genomes of all eukaryotes and play a critical role in altering gene expression and genome organization. In Drosophila melanogaster, transposable P elements are responsible for the phenomenon of hybrid dysgenesis. KP elements, a deletion-derivative of the complete P element, can suppress this mutagenic effect. KP elements can also silence the expression of certain other P-element-mediated transgenes in a process called P-element-dependent silencing (PDS), which is thought to involve the recruitment of heterochromatin proteins. To explore the mechanism of this silencing, we have mobilized KP elements to create a series of strains that contain single, well-defined KP insertions that show PDS. To understand the quantitative role of KP elements in PDS, these single inserts were combined in a series of crosses to obtain genotypes with zero, one, or two KP elements, from which we could examine the effect of KP gene dose. The extent of PDS in these genotypes was shown to be dose dependent in a logarithmic rather than linear fashion. A logarithmic dose dependency is consistent with the KP products interacting with heterochromatic proteins in a concentration-dependent manner such that two molecules are needed to induce gene silencing.

Protein kinase C potentiates cAMP-stimulated mouse duodenal mucosal bicarbonate secretion in vitro

2004 ◽  
Vol 286 (5) ◽  
pp. G814-G821 ◽  
Author(s):  
Bi-Guang Tuo ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett ◽  
Jon I. Isenberg
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Duodenal Mucosa ◽  
Bicarbonate Secretion ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ussing Chambers ◽  
Duodenal Bicarbonate Secretion

PKC has been shown to regulate epithelial Cl- secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current ( Isc). When PMA and dibutyryl-cAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc ( P > 0.05). However, a 1-h preincubation with PMA potentiated db-cAMP-stimulated duodenal bicarbonate secretion and Isc in a concentration-dependent manner (from 10-8 to 10-5M) ( P < 0.05). PMA preincubation had no effects on carbachol- or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKCα, -γ, -ϵ, -θ, -μ, and -ι/λ were expressed in murine duodenal mucosa. Ro 31–8220 (an inhibitor active against PKCϵ, -α, -β, and -γ), but not Gö 6983 (an inhibitor active against PKCα, -γ, -β, and -δ), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time- and concentration-dependently increased the activity of PKCϵ, an effect that was prevented by Ro 31–8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKCϵ isoform.

scholarly journals Sec1p directly stimulates SNARE-mediated membrane fusion in vitro

2004 ◽  
Vol 167 (1) ◽  
pp. 75-85 ◽  
Author(s):  
Brenton L. Scott ◽  
Jeffrey S. Van Komen ◽  
Hassan Irshad ◽  
Song Liu ◽  
Kirilee A. Wilson ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Membrane Fusion ◽  
Membrane Trafficking ◽  
Snare Complex ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Bud Neck ◽  
Precise Role

Sec1 proteins are critical players in membrane trafficking, yet their precise role remains unknown. We have examined the role of Sec1p in the regulation of post-Golgi secretion in Saccharomyces cerevisiae. Indirect immunofluorescence shows that endogenous Sec1p is found primarily at the bud neck in newly budded cells and in patches broadly distributed within the plasma membrane in unbudded cells. Recombinant Sec1p binds strongly to the t-SNARE complex (Sso1p/Sec9c) as well as to the fully assembled ternary SNARE complex (Sso1p/Sec9c;Snc2p), but also binds weakly to free Sso1p. We used recombinant Sec1p to test Sec1p function using a well-characterized SNARE-mediated membrane fusion assay. The addition of Sec1p to a traditional in vitro fusion assay moderately stimulates fusion; however, when Sec1p is allowed to bind to SNAREs before reconstitution, significantly more Sec1p binding is detected and fusion is stimulated in a concentration-dependent manner. These data strongly argue that Sec1p directly stimulates SNARE-mediated membrane fusion.

scholarly journals Peroxiredoxin 6 is required for blood vessel integrity in wounded skin

2007 ◽  
Vol 179 (4) ◽  
pp. 747-760 ◽  
Author(s):  
Angelika Kümin ◽  
Matthias Schäfer ◽  
Nikolas Epp ◽  
Philippe Bugnon ◽  
Christiane Born-Berclaz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Endothelial Cells ◽  
Ultrastructural Level ◽  
Peroxiredoxin 6 ◽  
Severe Hemorrhage ◽  
Vessel Integrity ◽  
Knockout Animals

Peroxiredoxin 6 (Prdx6) is a cytoprotective enzyme with largely unknown in vivo functions. Here, we use Prdx6 knockout mice to determine its role in UV protection and wound healing. UV-mediated keratinocyte apoptosis is enhanced in Prdx6-deficient mice. Upon skin injury, we observe a severe hemorrhage in the granulation tissue of knockout animals, which correlates with the extent of oxidative stress. At the ultrastructural level endothelial cells appear highly damaged, and their rate of apoptosis is enhanced. Knock-down of Prdx6 in cultured endothelial cells also increases their susceptibility to oxidative stress, thus confirming the sensitivity of this cell type to loss of Prdx6. Wound healing studies in bone marrow chimeric mice demonstrate that Prdx6-deficient inflammatory and endothelial cells contribute to the hemorrhage phenotype. These results provide insight into the cross-talk between hematopoietic and resident cells at the wound site and the role of reactive oxygen species in this interplay.

scholarly journals The role of nitrosative and oxidative stress in rainbow trout (Oncorhynchus mykiss) liver tissue applied mercury chloride (HgCl2)

2021 ◽  
Vol 38 (3) ◽  
pp. 269-273
Author(s):  
Mehmet Reşit Taysı ◽  
Muammer Kırıcı ◽  
Mahinur Kırıcı ◽  
Hasan Ulusal ◽  
Bünyamin Söğüt ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Liver Tissue ◽  
Stress Index ◽  
Mercury Chloride ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Total Antioxidant ◽  
Ld50 Value

The aim of this study was to determine oxidative stress caused by mercury chloride (HgCl2) in rainbow trout (Oncorhynchus mykiss) liver tissue. For this purpose, the LD50 value of HgCl2 on rainbow trout was determined as 551 μg/L. In the study, 40 fish in four groups were exposed to 25% and 50% (138 and 276 µg/L) of the two subletal doses of HgCl2 for 2 and 7 days, with 10 fish (n=10) in each group. To determine oxidative stress; peroxynitrite (ONOO−), total oxidant level (TOS), total antioxidant level (TAS), oxidative stress index (OSI) and malondialdehyde (MDA) were analyzed. In the study, it was observed that the differences between the groups in terms of ONOO−, TOS, TAS and OSI levels in the liver tissues was significant (P<0.05), however, this difference was not significant (P>0.05) in terms of MDA values. As a result, it can be concluded that HgCl2 increases ONOO−, TOS, TAS, OSI and MDA levels in liver tissue and even small doses of mercury are toxic to fish.

Abstract 40: Prothrombotic Role of Platelet Tlr2 in Hyperlipidemia

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Sudipta Biswas ◽  
Liang Xin ◽  
Soumya Panigrahi ◽  
Alejandro Zimman ◽  
Valentin Yakubenko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Platelet Reactivity ◽  
Biological Activities ◽  
Biologically Active ◽  
Dependent Manner ◽  
Prothrombotic State ◽  
Downstream Signaling ◽  
Subsequent Activation ◽  
Biologically Active Derivatives

A prothrombotic state and increased platelet reactivity are common in hyperlipidemia and oxidative stress. Lipid peroxidation, a major consequence of oxidative stress, generates highly reactive products including hydroxy-w-oxoalkenoic acids that modify autologous proteins generating biologically active derivatives. Phosphatidylethanolamine, the second most abundant eukaryotic phospholipid can also be modified by hydroxy-w-oxoalkenoic acids. However, the conditions leading to accumulation of such derivatives in circulation and their biological activities remain poorly understood. We now show that carboxyalkylpyrrole-phosphatidylethanolamine derivatives (CAP-PE) accumulate in plasma of hyperlipidemic ApoE -/- mice. CAP-PE directly bind to TLR2 and induce platelet integrin alpha 2b beta 3 activation and P-selectin expression in TLR2 dependent manner. Platelet activation by CAP-PE includes assembly of TLR2/TLR1 receptor complex, induction of downstream signaling via MyD88/TIRAP, phosphorylation of IRAK4, and subsequent activation of TRAF6. This in turn activates the Src family kinases, Syk and PLC gamma 2 and platelet integrins. By intravital thrombosis studies we have demonstrated that CAP-PE accelerate thrombosis in TLR2 dependent manner. Furthermore, we demonstrate that TLR2 deficient mice are protected from accelerated thrombosis induced by hyperlipidemia. Taken together, our studies demonstrate a cross-talk between innate immunity and integrin activation signaling pathways in platelets and reveal that TLR2 plays a key role in platelet hyperreactivity and prothrombotic state in hyperlipidemia.

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