In VivoTrapping of Nitric Oxide in the Brain of Neonatal Rats Treated with the HIV-1 Envelope Protein gp 120: Protective Effects of α-Phenyl-tert-butylnitrone

1996 ◽  
Vol 221 (2) ◽  
pp. 386-390 ◽  
Author(s):  
Tahereh Tabatabaie ◽  
Charles Stewart ◽  
Quentin Pye ◽  
Yashige Kotake ◽  
Robert A. Floyd
Keyword(s):  
Nitric Oxide ◽  
Envelope Protein ◽  
Protective Effects ◽  
Neonatal Rats ◽  
Gp 120 ◽  
The Brain ◽  
Hiv 1

Human Immunodeficiency Virus-1–Infected Macrophages Induce Inducible Nitric Oxide Synthase and Nitric Oxide (NO) Production in Astrocytes: Astrocytic NO as a Possible Mediator of Neural Damage in Acquired Immunodeficiency Syndrome

Blood ◽  
1999 ◽  
Vol 93 (6) ◽  
pp. 1843-1850 ◽  
Author(s):  
Kotaro Hori ◽  
Parris R. Burd ◽  
Keizo Furuke ◽  
Joseph Kutza ◽  
Karis A. Weih ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Human Immunodeficiency Virus ◽  
Inducible Nitric Oxide Synthase ◽  
Inos Expression ◽  
No Production ◽  
Immunodeficiency Virus ◽  
Oxide Synthase ◽  
The Brain ◽  
Hiv 1 ◽  
Inducible Nitric Oxide

Nitric oxide (NO) plays an important role in normal neural cell function. Dysregulated or overexpression of NO contributes to neurologic damage associated with various pathologies, including human immunodeficiency virus (HIV)-associated neurological disease. Previous studies suggest that HIV-infected monocyte-derived macrophages (MDM) produce low levels of NO in vitro and that inducible nitric oxide synthase (iNOS) is expressed in the brain of patients with neurologic disease. However, the levels of NO could not account for the degree of neural toxicity observed. In this study, we found that induction of iNOS with concomitant production of NO occurred in primary human astrocytes, but not in MDM, when astrocytes were cocultured with HIV-1–infected MDM. This coincided with decreased HIV replication in infected MDM. Supernatants from cocultures of infected MDM and astrocytes also stimulated iNOS/NO expression in astrocytes, but cytokines known to induce iNOS expression (interferon-γ, interleukin-1β, and tumor necrosis factor-) were not detected. In addition, the recombinant HIV-1 envelope protein gp41, but not rgp120, induced iNOS in cocultures of uninfected MDM and astrocytes. This suggests that astrocytes may be an important source of NO production due to dysregulated iNOS expression and may constitute one arm of the host response resulting in suppression of HIV-1 replication in the brain. It also leads us to speculate that neurologic damage observed in HIV disease may ensue from prolonged, high level production of NO.

scholarly journals Transgenic mice expressing HIV-1 envelope protein gp120 in the brain as an animal model in neuroAIDS research

2017 ◽  
Vol 24 (2) ◽  
pp. 156-167 ◽  
Author(s):  
Victoria E. Thaney ◽  
Ana B. Sanchez ◽  
Jerel A. Fields ◽  
Arpi Minassian ◽  
Jared W. Young ◽  
...  
Keyword(s):  
Animal Model ◽  
Transgenic Mice ◽  
Envelope Protein ◽  
Protein Gp120 ◽  
The Brain ◽  
Envelope Protein Gp120 ◽  
Hiv 1

Oxidative stress in the brain of nicotine-induced toxicity: protective role of Andrographis paniculata Nees and vitamin E

2009 ◽  
Vol 34 (2) ◽  
pp. 124-135 ◽  
Author(s):  
Subhasis Das ◽  
N. Gautam ◽  
Sankar Kumar Dey ◽  
Tarasankar Maiti ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Body Mass ◽  
Brain Mitochondria ◽  
Brain Regions ◽  
Protective Role ◽  
Andrographis Paniculata ◽  
Protective Effects ◽  
The Brain

Mitochondria are the crossroads of several crucial cellular activities; they produce considerable quantities of superoxide radical and hydrogen peroxide, which can damage important macromolecules. Nicotine affects a variety of cellular processes, from induction of gene expression to modulation of enzymatic activities. The aim of this study was to elucidate the protective effects of andrographolide (ANDRO) aqueous extract (AE-Ap) of Andrographis paniculata, and vitamin E on nicotine-induced brain mitochondria. In this investigation, nicotine (1 mg·kg body mass–1·day–1) was treated, for the period of 7 days, simultaneously with 2 A. paniculata products, ANDRO and AE-Ap (250 mg·kg body mass–1·day–1); and vitamin E (50 mg·kg body mass–1·day–1) was supplemented in different group of male Wistar rats. The activities of mitochondrial electron transport chain (Mito–ETC) complexes (I, II, III), nitric oxide production, superoxide anion, catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, and concentrations of reduced glutathione and oxidized glutathione were measured in discrete regions of brain (the cerebral hemisphere, cerebellum, diencephalons, and brain stem). The study revealed that nicotine inhibits the Mito–ETC complexes and produces nitric oxide, which suppressed the mitochondrial oxidative stress scavenger system in different brain regions. In these circumstances, lipid peroxidation and protein oxidation were noted in different discrete regions of brain mitochondria. ANDRO, AE-Ap, and vitamin E showed the protective potentiality against nicotine toxicity. The analysis of such alterations is important in determining the basis of normal dysfunction in the brain associated with nicotine toxicity, which could be ameliorated by A. paniculata and vitamin E, and may help to develop therapeutic means against nicotine-induced disorders.

The effect of melatonin on protein oxidation and nitric oxide in the brain tissue of hypoxic neonatal rats

2007 ◽  
Vol 29 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Sevgi Eskiocak ◽  
Filiz Tutunculer ◽  
Umit Nusret Basaran ◽  
Ali Taskiran ◽  
Erol Cakir
Keyword(s):  
Nitric Oxide ◽  
Brain Tissue ◽  
Protein Oxidation ◽  
Neonatal Rats ◽  
The Brain

scholarly journals Protective effects of Fragaria ananassa methanolic extract in a rat model of cadmium chloride-induced neurotoxicity

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Manal F. Elkhadragy ◽  
Rami B. Kassab ◽  
Dina Metwally ◽  
Rafa S. Almeer ◽  
Rewaida Abdel-Gaber ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glutathione Peroxidase ◽  
Brain Tissue ◽  
Cadmium Chloride ◽  
Methanolic Extract ◽  
Oxidative Enzymes ◽  
Protective Effects ◽  
Fragaria Ananassa ◽  
Neuronal Toxicity ◽  
The Brain

Cadmium (Cd) is a common environmental toxicant that has harmful effects on plants, animals, and humans. The present study evaluated the protective effects of Fragaria ananassa methanolic extract (SME) on cadmium chloride (CdCl2)-induced neuronal toxicity in rats. Male albino rats were intraperitoneally (i.p) injected with CdCl2 (6.5 mg/kg) for 5 days with or without the SME (250 mg/kg). We measured the levels of Cd, lipid peroxidation (LPO), nitric oxide, glutathione (GSH), and oxidative enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase, and glutathione reductase (GR) in the whole brain homogenate. Compared with the control group, the Cd-intoxicated group showed a marked increase in the brain levels of Cd, LPO, and nitric oxide and a decrease in the levels of GSH and all tested antioxidant enzymes. Compared with Cd-intoxicated rats, the rats pretreated with SME showed restoration of oxidative balance in the brain tissue. While the expression of brain SOD2, CAT, glutathione peroxidase 1, and GR was down-regulated in the Cd-treated group, the expression of these enzymes was up-regulated in rats pretreated with SME. In addition, administration of SME before CdCl2 increased the Bcl-2 expression, but significantly decreased the expression of Bax. Immunohistochemical analysis showed that compared with Cd-intoxicated rats, rats pretreated with SME showed a decrease in the protein expression of tumor necrosis factor α (TNF-α). Our findings indicate that SME protects the brain tissue from Cd-induced neuronal toxicity by improving the antioxidant system and increasing antiapoptotic and anti-inflammatory activities.

The Effects of the HIV-1 Envelope Protein gp120 on the Production of Nitric Oxide and Proinflammatory Cytokines in Mixed Glial Cell Cultures

1996 ◽  
Vol 172 (1) ◽  
pp. 77-83 ◽  
Author(s):  
Ling-Yuan Kong ◽  
Belinda C. Wilson ◽  
Michael K. McMillian ◽  
Guoying Bing ◽  
Pearlie M. Hudson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glial Cell ◽  
Cell Cultures ◽  
Proinflammatory Cytokines ◽  
Envelope Protein ◽  
Protein Gp120 ◽  
Envelope Protein Gp120 ◽  
Hiv 1 ◽  
Glial Cell Cultures

Localization of the cGMP-dependent protein kinases in relation to nitric oxide synthase in the brain

1999 ◽  
Vol 17 (1) ◽  
pp. 45-55 ◽  
Author(s):  
A.E.-D El-Husseini ◽  
J Williams ◽  
P.B Reiner ◽  
S Pelech ◽  
S.R Vincent
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Kinases ◽  
Dependent Protein ◽  
Oxide Synthase ◽  
The Brain

scholarly journals Comparing the protective effects of resveratrol, curcumin and sulforaphane against LPS/IFN-γ-mediated inflammation in doxorubicin-treated macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haidy A. Saleh ◽  
Eman Ramdan ◽  
Mohey M. Elmazar ◽  
Hassan M. E. Azzazy ◽  
Anwar Abdelnaser
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Raw 264.7 Cells ◽  
Inos Mrna ◽  
No Production ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Protective Effects ◽  
Tnf Α ◽  
Ifn Γ

AbstractDoxorubicin (DOX) chemotherapy is associated with the release of inflammatory cytokines from macrophages. This has been suggested to be, in part, due to DOX-mediated leakage of endotoxins from gut microflora, which activate Toll-like receptor 4 (TLR4) signaling in macrophages, causing severe inflammation. However, the direct function of DOX on macrophages is still unknown. In the present study, we tested the hypothesis that DOX alone is incapable of stimulating inflammatory response in macrophages. Then, we compared the anti-inflammatory effects of curcumin (CUR), resveratrol (RES) and sulforaphane (SFN) against lipopolysaccharide/interferon-gamma (LPS/IFN-γ)-mediated inflammation in the absence or presence of DOX. For this purpose, RAW 264.7 cells were stimulated with LPS/IFN-γ (10 ng/mL/10 U/mL) in the absence or presence of DOX (0.1 µM). Our results showed that DOX alone is incapable of stimulating an inflammatory response in RAW 264.7 macrophages. Furthermore, after 24 h of incubation with LPS/IFN-γ, a significant increase in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) mRNA levels was observed. Similarly, nitric oxide (NO) production and TNF-α and IL-6 protein levels were significantly upregulated. Moreover, in LPS/IFN-γ-treated macrophages, the microRNAs (miRNAs) miR-146a, miR-155, and miR-21 were significantly overexpressed. Interestingly, upon testing CUR, RES, and SFN against LPS/IFN-γ-mediated inflammation, only SFN was able to significantly reverse the LPS/IFN-γ-mediated induction of iNOS, TNF-α and IL-6 and attenuate miR-146a and miR-155 levels. In conclusion, SFN, at the transcriptional and posttranscriptional levels, exhibits potent immunomodulatory action against LPS/IFN-γ-stimulated macrophages, which may indicate SFN as a potential treatment for DOX-associated inflammation.

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