scholarly journals LIPOPOLYSACCHARIDE-INDUCED SYSTEMIC INFLAMMATORY RESPONSE ENHANCES THE DEVELOPMENT OF OXIDATIVE-NITROSATIVE STRESS IN SALIVARY GLANDS OF RATS UNDER ALCOHOL DAMAGE

2021 ◽  
Vol 67 (6) ◽  
pp. 60-67
Author(s):  
R.S. Kozaeva ◽  
◽  
M.O. Klymenko ◽  
V.О. Kostenko ◽  
◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Salivary Glands ◽  
Nitrosative Stress ◽  
Salmonella Typhi ◽  
No Synthase ◽  
Systemic Inflammatory Response ◽  
Aquaporin 5 ◽  
Superoxide Anion Production ◽  
Phagocyte Nadph Oxidase ◽  
Submandibular Salivary Glands

We addressed the role of lipopolysaccharide (LPS)-induced systemic inflammatory response (SIR) in the development of oxidative-nitrosative stress in the salivary glands of rats under the influence of alcohol. Ethanol (40%) at the dose of 24 mg/kg was administered intraperitoneally (ip) twice per day for 14 days. SIR was induced by ip administration of LPS (Salmonella typhi) at the dose 0.4 mg/kg for 1 week followed by a weekly LPS administration for 7 weeks. We found that long-term administration of ethanol in the back- ground of LPS-induced SIR increased the circulating level of proinflammatory markers (TNFa, IL-6) and C-reactive protein and this increase exceeded the respective values when LPS and alcohol were administered separately. Under these conditions, in submandibular salivary glands, the superoxide anion production by mitochondria respiratory chain was increased by 25.9 and 30.5%, by microsomal monooxygenases and NO synthase by 19.0 and 27,1%, by phagocyte NADPH-oxidase by 29.5 and 30.0%. The activity of inducible NO-synthase increased by 15.5 and 83.6%, the concentration of peroxynitrites of alkali and alkali-earth metals elevated by 32.5 and 58, 3%, and S- nitrosothiols raised by 20.2 and 22.7%. These changes were accompanied by a decrease in α-amylase activity and the aquaporin-5 concentration that impairs water and protein excretion by salivary glands. We conclude that adminis- tration of ethanol in the background of LPS-induced SIR results in more pronounced development of oxidative- nitrosative stress in the submandibular salivary glands and more marked dysfunction compared to separate use of LPS and alcohol.

scholarly journals EFFECT OF WATER-SOLUBLE QUERCETIN ON INDICATORS OF OXIDATIVE-NITROSATIVE STRESS IN TISSUES OF SUBMANDIBULAR SALIVARY GLANDS OF RATS UNDER LIPOPOLYSACCHARIDE-INDUCED SYSTEMIC INFLAMMATORY RESPONSE

2021 ◽  
Vol 21 (2) ◽  
pp. 175-181
Author(s):  
O.O. Shvaikovska ◽  
S.V. Denisenko ◽  
V.O. Kostenko
Keyword(s):  
Inflammatory Response ◽  
Salivary Glands ◽  
Nitrosative Stress ◽  
No Synthase ◽  
Systemic Inflammatory Response ◽  
Water Soluble ◽  
Male Rats ◽  
Soluble Form ◽  
Significant Shift ◽  
Submandibular Salivary Glands

The aim of this study was to investigate the effect of the water-soluble form of quercetin on the indicators of oxidative-nitrosative stress in the tissues of the submandibular salivary glands (SG) under conditions of lipopolysaccharide-induced systemic inflammatory response (SIR). The study was performed on 30 white Wistar male rats weighing 180-220 g, divided into 3 groups: 1st group included intact animals, 2nd group included animals, subjected to the systemic administration of lipopolysaccharide of Salmonella typhi, 3rd group involved animals, which received water-soluble quercetin complex with polyvinylpyrrolidone (corvitin) in a dosage of 100 mg/kg (10 mg/ g in terms of quercetin) intraperitoneally every 3 days, starting on the 30 day of the experiment with using S. typhi lipopolysaccharide. The latter was administered in a dose of 0.4 μg/kg body weight 3 times during the 1st week, and then once a week for the next 7 weeks. The study has demonstrated that applying quercetin under SIR restrains the production of reactive oxygen species in SG tissues: it reduces unstimulated production of superoxide anion radical and its induced generation with the administration of NADPH (by microsomes and NO-synthase), NADH (by mitochondria), S. typhi lipopolysaccharide (by leukocyte NADPH-oxidase). The administration of quercetin under SIR condition diminishes the signs of nitrosative stress in SG tissues, as evidenced by decrease in inducible NO-synthase activity without significant changes in ornithine decarboxylase activity and the level of coupling of constitutive isoform of NO-synthase, decreased concentration of highly active peroxynitrite, but, however, without significant shift in S-nitrosothiols content.

scholarly journals QUERCETIN LIMITS THE DEVELOPMENT OF OXIDATIVE-NITROSATIVE STRESS IN PERIODONTAL TISSUES IN DIFFERENT MODELS SIMULATING SYSTEMIC INFLAMMATORY RESPONSE

2019 ◽  
Vol 19 (4) ◽  
pp. 83-87
Author(s):  
A.M. Yelins’ka ◽  
S.M. Nazarenko ◽  
V.O. Kostenko
Keyword(s):  
Inflammatory Response ◽  
Nadph Oxidase ◽  
Nitrosative Stress ◽  
Soft Tissues ◽  
Salmonella Typhi ◽  
No Synthase ◽  
Systemic Inflammatory Response ◽  
Water Soluble ◽  
Soluble Form ◽  
Periodontal Tissues

The study was carried out to investigate the effect produced by water-soluble form of quercetin (corvitin) on the indices of the development of oxidative-nitrosative stress in periodontal soft tissues of rats subjected to systemic inflammatory response. This condition was simulated by using two models: one was induced by the Salmonella typhi lipopolysaccharide (LPS) administration (in a dose of 0.4 μg / kg of body wt three times through the 1st week and once a week for the next 7 weeks), as well as on the 14th day after a moderate craniocerebral injury (CCI). Applying corvitin in a dose of 500 μg / kg (10 μg / kg recalculated as quercetin) every third day starting from the 30th day of the experiment with the use of pyrogenalum reduced the production of superoxide anion radical (.О) by NADPH-dependent electron transport chains (endoplasmic reticulum and NO-synthase) by 18.1%, but did not considerably affect the mitochondrial chain. .О production by leukocyte NADPH-oxidase was by 16.7% lower. The total NO synthase (NOS) activity in periodontal tissues decreased by 40.6%, and the content of peroxynitrite ions was inferior to the relevant result of the group received pyrogenalum by 13.9%. Administration of corvitin in a dose of 500 mg/kg for 7 days after CCI modeling reduced the (.О) production by NADPH-dependent chains by 20.9%, and by mitochondria by 31.7% on the 14th day of post-traumatic period. .О production by leukocyte NADPH-oxidase was by 35.8% lower. NOS activity in periodontal tissues decreased by 45.8%, the content of peroxynitrite ions was inferior to the relevant value in the group with modeled CCI by 25.7%. This suggests the conclusion that applying water-soluble form of quercetin in conditions of systemic inflammatory response limits the signs of oxidative-nitrosative stress in periodontal soft tissues of rats.

Protection by mTOR Inhibition on Zymosan-Induced Systemic Inflammatory Response and Oxidative/Nitrosative Stress: Contribution of mTOR/MEK1/ERK1/2/IKKβ/IκB-α/NF-κB Signalling Pathway

Inflammation ◽  
2017 ◽  
Vol 41 (1) ◽  
pp. 276-298 ◽  
Author(s):  
Seyhan Sahan-Firat ◽  
Meryem Temiz-Resitoglu ◽  
Demet Sinem Guden ◽  
Sefika Pinar Kucukkavruk ◽  
Bahar Tunctan ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Nitrosative Stress ◽  
Systemic Inflammatory Response ◽  
Signalling Pathway ◽  
Mtor Inhibition ◽  
Stress Contribution

scholarly journals Death receptors mediate the adverse effects of febrile-range hyperthermia on the outcome of lipopolysaccharide-induced lung injury

2011 ◽  
Vol 301 (1) ◽  
pp. L60-L70 ◽  
Author(s):  
Anne B. Lipke ◽  
Gustavo Matute-Bello ◽  
Raquel Herrero ◽  
Venus A. Wong ◽  
Stephen M. Mongovin ◽  
...  
Keyword(s):  
Lung Injury ◽  
Inflammatory Response ◽  
Nitrosative Stress ◽  
Systemic Inflammatory Response ◽  
Alveolar Epithelial Cells ◽  
Receptor Activity ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Alveolar Permeability

We have shown that febrile-range hyperthermia enhances lung injury and mortality in mice exposed to inhaled LPS and is associated with increased TNF-α receptor activity, suppression of NF-κB activity in vitro, and increased apoptosis of alveolar epithelial cells in vivo. We hypothesized that hyperthermia enhances lung injury and mortality in vivo by a mechanism dependent on TNF receptor signaling. To test this, we exposed mice lacking the TNF-receptor family members TNFR1/R2 or Fas (TNFR1/R2−/−and lpr) to inhaled LPS with or without febrile-range hyperthermia. For comparison, we studied mice lacking IL-1 receptor activity (IL-1R−/−) to determine the role of inflammation on the effect of hyperthermia in vivo. TNFR1/R2−/−and lpr mice were protected from augmented alveolar permeability and mortality associated with hyperthermia, whereas IL-1R−/−mice were susceptible to augmented alveolar permeability but protected from mortality associated with hyperthermia. Hyperthermia decreased pulmonary concentrations of TNF-α and keratinocyte-derived chemokine after LPS in C57BL/6 mice and did not affect pulmonary inflammation but enhanced circulating markers of oxidative injury and nitric oxide metabolites. The data suggest that hyperthermia enhances lung injury by a mechanism that requires death receptor activity and is not directly associated with changes in inflammation mediated by hyperthermia. In addition, hyperthermia appears to enhance mortality by generating a systemic inflammatory response and not by a mechanism directly associated with respiratory failure. Finally, we observed that exposure to febrile-range hyperthermia converts a modest, survivable model of lung injury into a fatal syndrome associated with oxidative and nitrosative stress, similar to the systemic inflammatory response syndrome.

scholarly journals 26. Chronic periodontitis and endothelial dysfunction In patients with arterial hypertension

2021 ◽  
Vol 11 (4) ◽  
pp. 108-110
Author(s):  
Andrey Eremin ◽  
Alexandr Lepilin ◽  
Tatiana Lipatova
Keyword(s):  
Endothelial Dysfunction ◽  
Inflammatory Response ◽  
Arterial Hypertension ◽  
Clinical Examination ◽  
Chronic Periodontitis ◽  
No Synthase ◽  
Systemic Inflammatory Response ◽  
Endothelial No Synthase ◽  
Vasoactive Mediators

The work offers a view at the data obtained through an examination of 120 patients with chronic generalized periodontitis (CP) and arterial hypertension (AH). The check-up included clinical examination, immunohistochemical, morphometric studies, as well as evaluation of the endothelium vasodilating function. CP in patients with hypertension features more significant changes in the quantitative density of gum cells positive to ET-1, endothelial NO-synthase, if compared to the CP values in patients with no background somatic pathology. Changes affecting vasoactive mediators in the gum are associated with a systemic inflammatory response and a violation of the endothelium vasodilating function. Periodontitis remission can be achieved with the therapy of the neurotransmitter imbalance.

scholarly journals ROLE OF TRANSCRIPTIONAL FACTOR NF-κB IN DEVELOPMENT OF OXIDATIVE STRESS IN HEART OF RATS DURING SYSTEMIC INFLAMMATORY RESPONSE INDUCED BY BACTERIAL LIPOPOLYSACCHARIDE

2019 ◽  
Vol 19 (3) ◽  
pp. 108-112
Author(s):  
O.Ye. Akimov ◽  
A.Yu. Vetkina ◽  
A.I. Malyk ◽  
A.D. Shkodina ◽  
S.V. Denysenko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Inflammatory Response ◽  
Catalase Activity ◽  
No Synthase ◽  
Systemic Inflammatory Response ◽  
Bacterial Lipopolysaccharide ◽  
Male Rats ◽  
Nuclear Transcription Factor ◽  
Basic Production

Systemic inflammatory response syndrome (SIRS) is a threatening complication that can lead to myocardial infarction. Activation of the nuclear transcription factor κB (NF-κB) plays an unambiguous role in the SIRS development. The purpose of this study is to determine the effect of NF-κB nuclear transcription factor activation on production of superoxide anion radical (O2•-), superoxide dismutase (SOD) and catalase activity, concentration of free malondialdehyde (MDA) in the heart of rats during SIRS modelling. The experiment was performed on 24 mature Wistar male rats weighing 180-220 g. Animals were divided into 3 groups consisting of 8 animals (control, SIRS group, NF-κB blockade group). SIRS was modelled by intraperitoneal administration of bacterial lipopolysaccharide (Pyrogenal) in a dose of 0.4 μg / kg 3 times a week in the first week; then once a week for 2 months. The blockade of NF-κB was performed by administration of ammonium pyrrolidine dithiocarbamate (PDTC) in a dose of 76 mg / kg. Production of O2•-, activities of SOD and catalase, concentration of MDA was investigated in 10% heart tissues homogenate. Induction of SIRS by Pyrogenal increases basic production of O2•- by 54.6% compared to the control group. Production of O2•- by microsomal electron transport chain (ETC) and NO synthase increases by 52.9%; production of O2•- by mitochondrial ETC increases by 38,9%. Activity of SOD increases by 1.86 times, activity of catalase increases by 1.53 times. The concentration of free MDA in heart tissues has grown by 81.2%. Blockade of the transcription factor NF-κB reduces basic production of O2•- by 38.9%; by microsomal ETC and NO synthase by 41%; by mitochondrial ETC by 22.2% compared to SIRS group. SOD activity decreases by 56.7%, while catalase activity does not statistically significantly change. The concentration of free MDA in heart tissues decreases by 31.4%. Activation of the nuclear transcription factor NF-κB in the heart of rats during SIRS induced by Pyrogenal leads to an increase in O2•- production with subsequent development of oxidative stress. Compensatory activation of antioxidant enzymes under these conditions is not able to prevent the development of oxidative stress in heart tissues.

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