scholarly journals Quercetin Reduces Ehrlich Tumor-Induced Cancer Pain in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-18 ◽  
Author(s):  
Cassia Calixto-Campos ◽  
Mab P. Corrêa ◽  
Thacyana T. Carvalho ◽  
Ana C. Zarpelon ◽  
Miriam S. N. Hohmann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Pain ◽  
Analgesic Effect ◽  
Biological Effects ◽  
Neutrophil Recruitment ◽  
Mammary Adenocarcinoma ◽  
Myeloperoxidase Activity ◽  
Ehrlich Tumor ◽  
Nociceptive Responses ◽  
And Oxidative Stress

Cancer pain directly affects the patient’s quality of life. We have previously demonstrated that the subcutaneous administration of the mammary adenocarcinoma known as Ehrlich tumor induces pain in mice. Several studies have shown that the flavonoid quercetin presents important biological effects, including anti-inflammatory, antioxidant, analgesic, and antitumor activity. Therefore, the analgesic effect and mechanisms of quercetin were evaluated in Ehrlich tumor-induced cancer pain in mice. Intraperitoneal (i.p.) treatments with quercetin reduced Ehrlich tumor-induced mechanical and thermal hyperalgesia, but not paw thickness or histological alterations, indicating an analgesic effect without affecting tumor growth. Regarding the analgesic mechanisms of quercetin, it inhibited the production of hyperalgesic cytokines IL-1βand TNFαand decreased neutrophil recruitment (myeloperoxidase activity) and oxidative stress. Naloxone (opioid receptor antagonist) inhibited quercetin analgesia without interfering with neutrophil recruitment, cytokine production, and oxidative stress. Importantly, cotreatment with morphine and quercetin at doses that were ineffective as single treatment reduced the nociceptive responses. Concluding, quercetin reduces the Ehrlich tumor-induced cancer pain by reducing the production of hyperalgesic cytokines, neutrophil recruitment, and oxidative stress as well as by activating an opioid-dependent analgesic pathway and potentiation of morphine analgesia. Thus, quercetin treatment seems a suitable therapeutic approach for cancer pain that merits further investigation.

scholarly journals Apiaceae as an Important Source of Antioxidants and Their Applications

Cosmetics ◽  
2021 ◽  
Vol 8 (4) ◽  
pp. 111
Author(s):  
Punniamoorthy Thiviya ◽  
Ashoka Gamage ◽  
Dinushika Piumali ◽  
Othmane Merah ◽  
Terrence Madhujith
Keyword(s):  
Oxidative Stress ◽  
Biological Effects ◽  
Natural Antioxidants ◽  
Herbal Products ◽  
Oxidative Balance ◽  
Therapeutic Value ◽  
Wide Range ◽  
Ascorbic Acids ◽  
Beauty Care ◽  
And Oxidative Stress

The excess level of reactive oxygen species (ROS) disturbs the oxidative balance leading to oxidative stress, which, in turn, causes diabetes mellites, cancer, and cardiovascular diseases. These effects of ROS and oxidative stress can be balanced by dietary antioxidants. In recent years, there has been an increasing trend in the use of herbal products for personal and beauty care. The Apiaceae (previously Umbelliferae) family is a good source of antioxidants, predominantly phenolic compounds, therefore, widely used in the pharmaceutical, cosmetic, cosmeceutical, flavor, and perfumery industries. These natural antioxidants include polyphenolic acids, flavonoids, carotenoids, tocopherols, and ascorbic acids, and exhibit a wide range of biological effects, including anti-inflammatory, anti-aging, anti-atherosclerosis, and anticancer. This review discusses the Apiaceae family plants as an important source of antioxidants their therapeutic value and the use in cosmetics.

scholarly journals Huangkui Capsule Attenuates Lipopolysaccharide-Induced Acute Lung Injury and Macrophage Activation by Suppressing Inflammation and Oxidative Stress in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jinfang Deng ◽  
Zhenpeng He ◽  
Xiuru Li ◽  
Wei Chen ◽  
Ziwen Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Macrophage Activation ◽  
Neutrophil Infiltration ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Myeloperoxidase Activity ◽  
Tnf Α ◽  
And Oxidative Stress

Background. Huangkui capsule (HKC) comprises the total flavonoid extract of flowers of Abelmoschus manihot (L.) Medicus. This study aimed to explore the effects of HKC on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and LPS-stimulated RAW 264.7 cells. Methods. Enzyme-linked immunosorbent assay, histopathology, spectrophotometry, and quantitative real-time polymerase chain reaction were used for the assessments. Statistical analysis was performed using a one-way analysis of variance. Results. LPS significantly increased lung inflammation, neutrophil infiltration, and oxidative stress and downregulated lung miR-451 expression. Treatment with HKC dramatically attenuated the lung wet/dry weight ratio, reduced the total cell count in the bronchoalveolar lavage fluid (BALF), and inhibited myeloperoxidase activity in the lung tissues 24 h after LPS challenge. Histopathological analysis demonstrated that HKC attenuated LPS-induced tissue oedema and neutrophil infiltration in the lung tissues. Additionally, the concentrations of tumour necrosis factor- (TNF-) α and interleukin- (IL-) 6 in BALF and IL-6 in the plasma reduced after HKC administration. Moreover, HKC could enhance glutathione peroxidase and catalase activities and upregulate the expression of miR-451 in the lung tissues. In vitro experiments revealed that HKC inhibited the production of nitric oxide, TNF-α, and IL-6 in LPS-induced RAW 264.7 cells and mouse primary peritoneal macrophages. Additionally, HKC downregulated LPS-induced transcription of TNF-α and IL-6 in RAW 264.7 cells. Conclusions. These findings suggest that HKC has anti-inflammatory and antioxidative effects that may protect mice against LPS-induced ALI and macrophage activation.

Effects of Atorvastatin Combined with Nano-Selenium on Blood Lipids and Oxidative Stress in Atherosclerotic Rats

2021 ◽  
Vol 21 (2) ◽  
pp. 1331-1337
Author(s):  
Zhe Han ◽  
Yang Wang ◽  
Jing Li
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Endothelial Cell ◽  
High Efficiency ◽  
Biological Effects ◽  
Lipid Lowering ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Combined Use ◽  
And Oxidative Stress

Dyslipidemia and oxidative stress injury of blood vessel walls play important roles in the formation of atherosclerosis (AS) and plaque progression. This is also the main pathological basis for atherosclerosis. Statins, as inhibitors of HMG-CoA reductase in the process of cholesterol biosynthesis, have become key drugs for lipid-lowering treatment. Many studies have found the anti-atherosclerotic effect of atorvastatin is far beyond the lipid-lowering effect. Its lipid-lowering effects are also involved, such as anti-inflammatory, inhibiting endothelial cell ROS production, and improving endothelial cell damage. Nano selenium (Nano-Se) shows stronger anti-oxidation ability, lower toxicity, high efficiency absorption and strong immune regulation ability. Because of the unique biological effects of Nano-Se, it has broad prospects in the field of human health care. Therefore, in this study, by constructing a rat model of abnormal lipid metabolism, we observed changes in parameters such as serum peroxidase (MPO), propylene glycol (MDA), superoxide dismutase (SOD), and blood lipid levels in atherosclerotic rats Happening, furthermore, the effects of atorvastatin+nano-selenium on lipid metabolism disorders and the protective effects and mechanisms of oxidative stress injury in rats were investigated and with a view to providing new targets for the treatment of arteriosclerosis. The results of this study demonstrated that contrast to the AS rat, the combined use of atorvastatin+nano-selenium group could significantly reduce serum TC, TG, and LDL-C contents, and declined tissue lesions such as aortic arch and liver; Significantly enhanced the activities of GPx-1 and SOD in serum, decreased MDA content, and increased the SOD activity in rat aorta. These results suggested that the combined use of atorvastatin+nano-selenium has good protection against oxidative stress caused by disorders of lipid metabolism.

scholarly journals Oxidative stress induces cell death partially by decreasing both mRNA and protein levels of nicotinamide phosphoribosyltransferase in differentiated PC12 cells

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11401
Author(s):  
Cuiyan Zhou ◽  
Weihai Ying
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Neurological Diseases ◽  
Biological Effects ◽  
Stress Conditions ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Differentiated Pc12 Cells ◽  
And Oxidative Stress

Background. Multiple studies have indicated crucial roles of NAD+ deficiency in several neurological diseases and aging. It is critical to discover the mechanisms underlying the NAD+ deficiency. A decreased level of Nicotinamide phosphoribosyltransferase (Nampt)—an important enzyme in the salvage pathway of NAD+ synthesis—has been found under certain pathological conditions, while the mechanisms underlying the Nampt decrease are unclear. The purpose of this study is to test the hypothesis that oxidative stress can produce decreased Nampt, and to investigate the biological effects of Nampt on NAD+ synthesis and cell survival under both basal and oxidative stress conditions. Methods. We used differentiated PC12 cells as a cellular model to investigate the effects of oxidative stress on the levels of Nampt. Multiple assays, including flow cytometry-based cell death assays and NAD+ assays were conducted. Results. First, oxidative stress can decrease the levels of Nampt mRNA and Nampt protein; second, Nampt plays significant roles in NAD+ synthesis under both basal conditions and oxidative stress conditions; third, Nampt plays critical roles in cell survival under both basal conditions and oxidative stress conditions; and fourth, oxidative stress produced decreased NAD+ levels and cell survival partially by decreasing Nampt. Collectively, our study has indicated that oxidative stress is a pathological factor leading to decreased Nampt, which plays important roles in oxidative stress-produced decreases in NAD+ levels and cell survival. Our findings have indicated major roles of Nampt in maintaining NAD+ levels and cell survival under both basal and oxidative stress conditions.

scholarly journals NK-1 antagonist reduces colonic inflammation and oxidative stress in dextran sulfate-induced colitis in rats

2000 ◽  
Vol 279 (6) ◽  
pp. G1298-G1306 ◽  
Author(s):  
Arthur F. Stucchi ◽  
Scott Shofer ◽  
Susan Leeman ◽  
Olivier Materne ◽  
Eve Beer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ulcerative Colitis ◽  
Disease Activity ◽  
Chronic Ulcerative Colitis ◽  
Tissue Damage ◽  
Intraperitoneal Administration ◽  
Myeloperoxidase Activity ◽  
Colonic Tissue ◽  
Colonic Inflammation ◽  
And Oxidative Stress

Although substance P (SP) has been implicated as a mediator of neurogenic inflammation in the small intestine, little information is available regarding the role of SP in the pathogenesis of chronic ulcerative colitis. In this study, our aim was to investigate whether the intraperitoneal administration of a nonpeptide neurokinin-1 (NK-1) antagonist, CP-96345, which antagonizes the binding of SP to its NK-1 receptor, results in the attenuation of colonic inflammation induced in rats by 5% dextran sodium sulfate (DSS) in drinking water for 10 days compared with an inactive enantiomer, CP-96344. Disease activity was assessed daily for 10 days, after which colonic tissue damage was scored and myeloperoxidase activity and colon and urinary 8-isoprostanes were measured. Animals receiving DSS exhibited marked physical signs of colitis by day 5 compared with controls. Chronic administration of the NK-1 antagonist significantly reduced the disease activity index, mucosal myeloperoxidase activity, colonic tissue damage score, and mucosal and urinary levels of 8-isoprostanes compared with inactive enantiomer- or vehicle-injected (saline) animals receiving DSS alone. These data indicate that the administration of an NK-1 antagonist can attenuate colonic inflammation and oxidative stress and suggest a novel therapeutic approach in the treatment of chronic ulcerative colitis.

Serum myeloperoxidase activity and oxidative stress in patients with acute brucellosis

2012 ◽  
Vol 45 (10-11) ◽  
pp. 733-736 ◽  
Author(s):  
Mustafa Kasım Karahocagil ◽  
Mehmet Aslan ◽  
Mehmet Resat Ceylan ◽  
Aytekin Cıkman ◽  
Mahmut Sunnetcioglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myeloperoxidase Activity ◽  
And Oxidative Stress

scholarly journals Biological effects induced by Gadolinium nanoparticles on Lymphocyte A20 cell line

2017 ◽  
Vol 1 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Cecilia Virginia Gheran ◽  
Sorina Nicoleta Voicu ◽  
Guillaume Rigaux ◽  
Maite Callewaert ◽  
Francoise Chuburu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biological Effects ◽  
Reactive Oxygen Species Generation ◽  
Antioxidant Defense System ◽  
Dependent Manner ◽  
Lactate Dehydrogenase Activity ◽  
In Vitro Effects ◽  
Dose Dependent ◽  
And Oxidative Stress

Abstract Gadolinium nanoparticles (GdNPs) are potential agents for MRI of lymph nodes. The aim of this study was to evaluate the in vitro effects of 1 μM, 2.5 μM and 5 μM of GdDOTA⊂CS-TPP/HA and GdDOTP⊂CS-TPP/HA NPs on A20 lymphocyte cells exposed for 6 and 24 hours. The total cellular biomass (SRB), lactate dehydrogenase activity (LDH) and oxidative stress parameters, such as reactive oxygen species generation (ROS), reduced glutathione (GSH), malondialdehyde (MDA) and advanced oxidation protein products (AOPP) were analyzed by spectrophotometric and fluorimetric methods. After cells exposure to 1 μM, 2.5 μM and 5 μM of GdDOTP⊂CS-TPP/HA NPs their viability decreased in a time- and dose-dependent manner, whereas for GdDOTA⊂CS-TPP/HA no significant changes were noticed. Both NPs formulations in doses of 1 μM, 2.5 μM, 5 μM did not affect the plasma membrane at each time point tested. The levels of ROS, MDA and AOPP increased proportionally with the concentration and exposure time. GSH concentration decreased significantly for all doses of both NPs tested. Taken together our data suggest that, GdDOTP⊂CS-TPP/HA and GdDOTA⊂CS-TPP/HA NPs induced oxidative stress in A20 lymphocyte cells which was counteracted by the cells antioxidant defense system to a certain extend.

scholarly journals Proinflammatory and Oxidative Stress Markers in Patients with Periodontal Disease

2007 ◽  
Vol 2007 ◽  
pp. 1-5 ◽  
Author(s):  
Ivan Borges Jr. ◽  
Emília Addison Machado Moreira ◽  
Danilo Wilhem Filho ◽  
Tiago Bittencourt de Oliveira ◽  
Marcelo Barreto Spirelle da Silva ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Periodontal Disease ◽  
Gingival Tissue ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Enzymatic Antioxidants ◽  
Oxidative Stress Markers ◽  
Oxidative Stress Biomarkers ◽  
Stress Markers ◽  
And Oxidative Stress

Objective. To evaluate the involvement of proinflammatory and oxidative stress markers in gingival tissue in individuals with chronic periodontitis.Subject and methods. Eighteen subjects were divided in two groups: experimental (age52.9±5.0) and control (age51.1±9.6). The activities of enzymatic antioxidants such as catalase, glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase, nonenzymatic antioxidants: total glutathione and reduced glutathione, oxidized glutathione (GSSG), thiobarbituric acid reactive substances (TBARS), and myeloperoxidase activity (MPO) were evaluated in gingival tissues from interproximal sites. Statistical differences between groups were determined by independent Studentttest andP<.05.Results. Individuals with periodontal disease exhibited a significant increase in the activities of MPO, GPx, GST, and also in TBARS and GSSG levels in gingival tissue compared to the control group (P<.05).Conclusion. The results of the present work showed an important correlation between oxidative stress biomarkers and periodontal disease.

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