scholarly journals Effects of Pristane Alone or Combined with Chloroquine on Macrophage Activation, Oxidative Stress, and Th1/Th2 Skewness

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Qiufang Ouyang ◽  
Ziyang Huang ◽  
Zhenhua Wang ◽  
Xiaoqing Chen ◽  
Jingqin Ni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biochemical Parameters ◽  
Macrophage Activation Syndrome ◽  
Macrophage Activation ◽  
Lactic Dehydrogenase ◽  
Peritoneal Macrophages ◽  
Protective Role ◽  
Hematological And Biochemical Parameters

We investigated the protective role of chloroquine against pristane-induced macrophage activation, oxidative stress, and Th1/Th2 skewness in C57BL/6J mice. Those mice were treated with pristane alone or combined with chloroquine. Hematological and biochemical parameters, macrophage phagocytic function, the oxidant/antioxidant index, cytokine for IFN-γ, TNF-α, IL-4, and IL-6, and the isotypes of IgG2a and IgG1 were determined. And the expression of T-bet/GATA-3 and IL-12/IL-10 mRNA in spleen were analyzed by real-time PCR. We found that pristane treatment for a period of 12 or 24 weeks triggered macrophage activation syndrome, characterized by hemophagocytosis in spleen and peripheral blood, enhanced lipid phagocytosis by peritoneal macrophages in vitro, erythropenia and leucopenia, increased anti-Smith, lactic dehydrogenase, triglyceride, and ferritin, as well as hypercytokinemia of IFN-γ, TNF-α, IL-4, and IL-6. In parallel, a significant increase in lipid peroxidation and a decrease in superoxide dismutase, glutathione, and catalase activity, as well as a skewed Th1/Th2 balance in spleen, were observed. However, chloroquine supplementation showed a remarkable amelioration of these abnormalities. Our data indicate that pristane administration induces macrophage activation, oxidative stress, and Th1/Th2 skewness, which can be attenuated by chloroquine.

scholarly journals A Protective Role of Paeoniflorin in Fluctuant Hyperglycemia-Induced Vascular Endothelial Injuries through Antioxidative and Anti-Inflammatory Effects and Reduction of PKCβ1

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jing-Shang Wang ◽  
Ye Huang ◽  
Shuping Zhang ◽  
Hui-Jun Yin ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Umbilical Vein ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Glucose Levels ◽  
Umbilical Vein Endothelial Cells

Hyperglycemia fluctuation is associated with diabetes mellitus (DM) complications when compared to persistent hyperglycemia. Previous studies have shown that paeoniflorin (PF), through its antiapoptosis, anti-inflammation, and antithrombotic properties, effectively protects against cardiovascular and cerebrovascular disease. However, the mechanism underlying the protection from PF against vascular injuries induced by hyperglycemia fluctuations remains poorly understood. Herein, we investigated the potential protective role of PF on human umbilical vein endothelial cells (HUVECs) subjected to intermittent glucose levels in vitro and in DM rats with fluctuating hyperglycemia in vivo. A remarkable increased apoptosis associated with elevated inflammation, increased oxidative stress, and high protein level of PKCβ1 was induced in HUVECs by intermittently changing glucose for 8 days, and PF recovered those detrimental changes. LY333531, a potent PKCβ1 inhibitor, and metformin manifested similar effects. Additionally, in DM rats with fluctuating hyperglycemia, PF protected against vascular damage as what has been observed in vitro. Taken together, PF attenuates the vascular injury induced by fluctuant hyperglycemia through oxidative stress inhibition, inflammatory reaction reduction, and PKCβ1 protein level repression, suggesting its perspective clinical usage.

scholarly journals Manganese Induces Oxidative Stress, Redox State Unbalance and Disrupts Membrane Bound ATPases on Murine Neuroblastoma Cells In Vitro: Protective Role of Silymarin

2011 ◽  
Vol 36 (8) ◽  
pp. 1546-1557 ◽  
Author(s):  
Yassine Chtourou ◽  
Khaled Trabelsi ◽  
Hamadi Fetoui ◽  
Ghada Mkannez ◽  
Héla Kallel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox State ◽  
Neuroblastoma Cells ◽  
Protective Role ◽  
Murine Neuroblastoma ◽  
Membrane Bound

Inhibition of salivary enzymes by cigarette smoke and the protective role of glutathione

2002 ◽  
Vol 21 (1) ◽  
pp. 7-11 ◽  
Author(s):  
B Zappacosta ◽  
S Persichilli ◽  
A Mordente ◽  
A Minucci ◽  
D Lazzaro ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Periodontal Diseases ◽  
Lactic Dehydrogenase ◽  
Protective Role ◽  
Significant Inhibition ◽  
Enzymatic Activities ◽  
Enzyme Molecules

Tobacco smoke is involved in the pathogenesis of several diseases regarding different body systems, mainly cardiovascular and respiratory in addition to its local toxic effect in the oral cavity. The noxious effects of smoke compounds justify the high incidence of periodontal diseases, caries, and neoplastic diseases of oral tissues in smokers. Some toxic components of tobacco smoke, unsaturated and saturated aldehydes, could interact with thiol rich compounds, leading to structural and functional modification of these molecules. Previous papers have demonstrated an in vitro significant decrease of some enzymatic activities, both in plasma and in saliva, following external addition of aldehydes or exposure to cigarette smoke (CS). Furthermore, the same studies underlined the protective effect exerted by the addition of glutathione (GSH) against the damaging role of smoke aldehydes. In this study some salivary enzymes (lactic dehydrogenase [LDH], aspartate aminotransferase [AST] and amylase), and total GSH were measured in 20 volunteers smokers, before and just after smoking a single cigarette. All enzymatic activities showed a significant inhibition following a single cigarette, probably due to the interaction between smoke aldehydes and–SH groups of the enzyme molecules. Moreover, the percentage of the enzymatic inhibition showed a negative correlation with the basal level of salivary GSH. Our results emphasize that not only one cigarette is sufficient to impair the salivary enzymatic activities but also strengthen the proposed protective role of GSH against the noxious biochemical effects of CS.

scholarly journals Fucoidan Protects against Acute Sulfoxaflor-Induced Hematological/Biochemical Alterations and Oxidative Stress in Male Mice

2021 ◽  
Vol 15 (1) ◽  
pp. 16
Author(s):  
Petek Piner Benli ◽  
Merve Kaya ◽  
Yusuf Kenan Dağlıoğlu
Keyword(s):  
Oxidative Stress ◽  
Biochemical Parameters ◽  
Biological Activities ◽  
Hematological Parameters ◽  
Sulfated Polysaccharide ◽  
Protective Role ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Hematological And Biochemical Parameters ◽  
And Oxidative Stress

Fucoidan is a sulfated polysaccharide which can be found among a number of macroalgea species. It has a broad spectrum of biological activities including anti-oxidant, anti-tumor, immunoregulation, anti-viral and anti-coagulant. The current study was performed to investigate possible protective effects of fucoidan for sulfoxaflor-induced hematological/biochemical alterations and oxidative stress in the blood of male Swiss albino mice. For this purpose, sulfoxaflor was administered at a dose of 15 mg/kg/day (1/50 oral LD50), and fucoidan was administered at a dose of 50 mg/kg/day by oral gavage alone and combined for 24 h and 7 days. Hematological parameters (RBC, HGB, HCT, MCV, MCH, MCHC, Plt, WBC, Neu, Lym and Mon), serum biochemical parameters (AST, ALT, GGT, LDH, BUN, Cre and TBil), and serum oxidative stress/antioxidant markers (8-OHdG, MDA, POC and GSH) were analyzed. The results indicated that sulfoxaflor altered hematological and biochemical parameters and caused oxidative stress in mice; fucoidan ameliorated some hematological and biochemical parameters and exhibited a protective role as an antioxidant against sulfoxaflor-induced oxidative stress.

scholarly journals The antioxidant effects of melatonin in blood platelets during exposure to electromagnetic radiation – an in vitro study

2021 ◽  
Vol 75 (1) ◽  
pp. 889-895
Author(s):  
Małgorzata Lewicka ◽  
Magdalena Zawadzka ◽  
Gabriela Henrykowska ◽  
Maciej Rutkowski ◽  
Andrzej Buczyński
Keyword(s):  
Oxidative Stress ◽  
Electromagnetic Radiation ◽  
Blood Platelets ◽  
In Vitro Study ◽  
Oxygen Metabolism ◽  
Protective Role ◽  
Negative Effect ◽  
Antioxidant Effects

Abstract Objectives The article presents the results of an in vitro study aimed at identifying changes in parameters of oxidative stress – concentration of malondialdehyde (MDA), enzymatic activity of superoxide dismutase (SOD-1) and protective antioxidant role of melatonin (MLT) during the exposure of blood platelets to electromagnetic radiation (EMR) emitted by monitors. Methods Platelets were exposed to an EMR for 30- and 60 min. generated by monitors (1 kHz frequency, 220 V/m intensity). In each sample the level of SOD-1 activity and concentration of MDA were determined. Results The MDA concentration increased significantly after 30-and 60-min. irradiation, as compared to control values (2.53 vs 1.36; 3.64 vs 1.36 nmol/109 blood platelets) and after the addition of MLT it decreased (2.53 vs 1.55; 3.64 vs 1.12 nmol/109 blood platelets). The activity of SOD-1 increased significantly compared to control values after 30 min. and 60 min. of exposure to EMR (1.97vs 0.75; 2.08 vs 0.75 U/g of protein), and significantly decreased after the addition of MLT only in samples exposed for 60 min. (2.08 vs 0.95 U/g of protein). Discussion The results demonstrated the possibly negative effect of EMR on oxygen metabolism of blood platelets and indicated a possible protective role of melatonin in this process.

Pipecolic acid induces oxidative stress in vitro in cerebral cortex of young rats and the protective role of lipoic acid

2013 ◽  
Vol 29 (1) ◽  
pp. 175-183 ◽  
Author(s):  
Giovana Reche Dalazen ◽  
Melaine Terra ◽  
Carlos Eduardo Diaz Jacques ◽  
Juliana G. Coelho ◽  
Raylane Freitas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Lipoic Acid ◽  
Protective Role ◽  
Pipecolic Acid ◽  
Young Rats

scholarly journals Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α2-Adrenergic Receptor-Dependent Suppression of Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Peibiao Lv ◽  
Tufeng Chen ◽  
Peibin Liu ◽  
Lei Zheng ◽  
Jingling Tian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Orthotopic Liver Transplantation ◽  
Adrenergic Receptor ◽  
Protective Role ◽  
Intestinal Injury ◽  
Protective Effects ◽  
Barrier Dysfunction

Patients with orthotopic liver transplantation (OLT) frequently develop acute gut injury (AGI), and dexmedetomidine (Dex) has been reported to exert a protective effect against AGI. We investigated whether Dex protects against AGI through antioxidative stress effects by the Nrf2/HO-1 antioxidative signaling pathway. Rats were randomly allocated into a sham group and six orthotopic autologous liver transplantation (OALT) groups receiving different doses of Dex together with/without α2-adrenergic receptor (AR) blockers. Intestinal tissues were collected to visualize the barrier damage and to measure the indexes of oxidative stress. For in vitro studies, rat intestinal recess epithelial cells (IEC-6) underwent hypoxia/reoxygenation (H/R), and the protective role of Dex was evaluated after α2A-AR siRNA silencing. OALT resulted in increased oxidative stress, significant intestinal injury, and barrier dysfunction. Dex attenuated OALT-induced oxidative stress and intestinal injury, which was abolished by the pretreatment with the nonspecific α2A-AR siRNA blocker atipamezole and the specific α2A-AR siRNA blocker BRL-44408, but not by the specific 2B/C-AR siRNA blocker ARC239. Silencing of α2A-AR siRNA also attenuated the protective role of Dex on alleviating oxidative stress in IEC-6 cells subjected to H/R. Dex exerted its protective effects by activating Nrf2/HO-1 antioxidative signaling. Collectively, Dex attenuates OALT-induced AGI via α2A-AR-dependent suppression of oxidative stress, which might be a novel potential therapeutic target for OALT-induced AGI.

Boron Compounds Counteracts Oxidative Stress Mediated Genotoxicity Induced by Fe3O4 Nanoparticles In Vitro

2016 ◽  
Vol 835 ◽  
pp. 84-90 ◽  
Author(s):  
Hasan Türkez ◽  
Erdal Sönmez ◽  
Abdulgani Tatar
Keyword(s):  
Oxidative Stress ◽  
Boric Acid ◽  
Antioxidant Capacity ◽  
Blood Cells ◽  
Defense Mechanisms ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Boron Compounds

Due to rapid growing of nanotechnology, it is currently being used in many areas including biotechnology, electronics, drug delivery systems, cosmetics, material science and biosensors. Oxidative stress is considered as main cause behind the toxicity of nanoparticles (NPs). Recent reports indicate that boron is effective in protecting cells or organisms against oxidative damages by enhancing antioxidant defense mechanisms. However, protective role of boron compounds in nanotoxicity is not investigated yet. Therefore we assessed the potential protective role of boric acid (BA) and borax (BX) against the toxic responses of nano-Fe3O4 particles (IO NPs) in cultured human whole blood cells. Our results showed that IO NPs induced genotoxicity in human lymphocytes demonstrated by sister chromatid exchange (SCE) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) assays. Again, IO NPs caused decreases of total antioxidant capacity (TAC) and decreases of total oxidative stress (TOS) levels in vitro. Co-application of boric acid and borax (2.5 to 10 ppm) into the cell cultures significantly ameliorated genotoxicity and oxidative stress caused by IO NPs. In a conclusion, this study is the first report revealing that BA and BX significantly protected human blood cells from the toxicity of IO NPs, which is mediated through the generation of oxidative stress and depletion of antioxidant capacity.

scholarly journals Oxidative Stress in Graves Disease and Graves Orbitopathy

2020 ◽  
Vol 9 (Suppl. 1) ◽  
pp. 40-50
Author(s):  
Giulia Lanzolla ◽  
Claudio Marcocci ◽  
Michele Marinò
Keyword(s):  
Oxidative Stress ◽  
Clinical Studies ◽  
Therapeutic Option ◽  
Protective Role ◽  
Beneficial Effects ◽  
Antioxidant Agents ◽  
Graves Orbitopathy

Oxidative stress is involved in the pathogenesis of Graves hyperthyroidism (GH) and Graves orbitopathy (GO) and an antioxidant approach has been proposed for both. In GH, a disbalance of the cell redox state is associated with thyroid hyperfunction and antithyroid medications may reduce oxidative stress. Tissue hypoxia participates in the pathogenesis of GO, and oxygen free radicals are involved in the typical changes of orbital tissues as reported by in vitro and clinical studies. Antioxidant agents, especially selenium, have been proposed as a therapeutic option for GH and GO. A clinical study regarding the use of selenium in mild GO has provided evidence for a beneficial effect in the short term, even though its beneficial effects in the long term are still to be investigated. In addition to selenium, a protective role of other antioxidant agents, i.e., quercetin, enalapril, vitamin C, <i>N</i>-acetyl-L-cysteine and melatonin has been suggested by in vitro studies, although clinical studies are lacking. Here, we review the role of oxidative stress and antioxidant agents in GH and GO.

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