scholarly journals Zygophyllum album aqueous extract reduces oxidative damage in erythrocytes and attenuates pro-inflammatory markers in hypercholesterolemic-diabetic rats

2020 ◽  
Vol 09 (02) ◽  
pp. 106-116
Author(s):  
Yasmina BAHLIL ◽  
◽  
Djamil KROUF ◽  
Nawal TALEB-DIDA
Keyword(s):  
Protein C ◽  
Diabetic Rats ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Long Time ◽  
Male Wistar Rats ◽  
Antioxidant Enzymes Activities ◽  
Factor Α ◽  
Radical Attack ◽  
Necrosis Factor

Introduction. Zygophyllum album (Z. album) is used in traditional medicine for a long time for its anti-diabetic activities. Objective. To investigate Z. album extract supplementation effects on redox and inflammatory status in hypercholesterolemic-diabetic rats. Material and methods. Male Wistar rats (n=36), weighing 200±10g were divided into three groups (n=12). The 1st group was hypercholesterolemic (HC) by consuming cholesterol enriched diet (1%). The 2nd group was diabetic (D) by intraperi-toneal injection of streptozotocin (STZ) (35 mg/kg body weight). The 3rd group was hypercholesterolemic-diabetic (HC-D). Each group was divided into two subgroups (n=6), untreated (HC, D, HC-D) and treated groups with 1% Z. album extract (HC-Za, D-Za and HC-D-Za). Results. At d28, Z. album treatment lead to a decrease in erythrocytes thiobarbituric reactive substances (TBARS) in HC-Za (-44%), D-Za (-66%) and HC-D-Za (-23%) groups. Increased erythrocytes antioxidant enzymes activities (superoxide dismu-tase, glutathione peroxidase, glutathione reductase and catalase) were observed in HC-Za, D-Za and HC-D-Za (p<0.05). In plasma, interleukin (IL-1 β and IL-6) concentrations were reduced by -44, -50 and -33%, and -49, 38 and -41%, respectively in treated groups. In plasma, a decrease of TNF-α (Tumor Necrosis Factor-α), homocysteine and protein-C reactive (CRP) was observed in Z. album treated groups (p<0.05). Conclusion. Z. album reduces radical attack and improves anti-inflammatory proprieties in hypercholesterolemic-diabetic rats.

TNF-α induced bronchial vasoconstriction

2000 ◽  
Vol 279 (3) ◽  
pp. H946-H951 ◽  
Author(s):  
Elizabeth M. Wagner
Keyword(s):  
Bronchial Artery ◽  
Autologous Blood ◽  
Inflammatory Status ◽  
Tnf Α ◽  
In Vitro Systems ◽  
Essential Function ◽  
Factor Α ◽  
Necrosis Factor ◽  
Airways Inflammation

The pro-inflammatory characteristics of tumor necrosis factor-α (TNF-α) have been extensively characterized in in vitro systems. Furthermore, this cytokine has been shown to play a pivotal role in airways inflammation in asthma. Since the airway vasculature also performs an essential function in inflammatory cell transit to the airways, experiments were performed to determine the effects of TNF-α on bronchial vascular resistance (BVR). In anesthetized, ventilated sheep, the bronchial artery (BA) was cannulated and perfused with autologous blood. BVR was defined as inflow pressure/flow and averaged 6.3 ± 0.2 mmHg · ml−1 · min−1 (±SE) for the 25 sheep studied. Recombinant human TNF-α (10 μg for 20 or 40 min) infused directly into the BA resulted in a significant decrease in BVR to 87% of baseline ( P < 0.05). This vasodilation was followed by a reversal of tone by 120 min and a sustained increase in BVR to 126% of baseline ( P < 0.05). Since others have shown TNF-α caused coronary vasoconstriction through endothelial release of endothelin-1 (ET-1), an ET-1 antagonist was used to block bronchial vasoconstriction. BQ-123, a selective ETA receptor antagonist, was delivered to the bronchial vasculature prior to TNF-α challenge. Attenuation of bronchial vasoconstriction was observed at 120 min ( P < 0.03). Thus TNF-α causes bronchial vasoconstriction by the secondary release of ET-1. Although TNF-α exerts pro-inflammatory actions on most cells of the airways, vasoactive properties of this cytokine likely further contribute to the inflammatory status of the airways.

Regulation of Murine Protein C Gene Expression In Vivo: Effects of Tumor Necrosis Factor-α, Interleukin-1, and Transforming Growth Factor-β

1999 ◽  
Vol 82 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
Takayoshi Shimokawa ◽  
Tetsuhito Kojima ◽  
David Loskutoff ◽  
Hidehiko Saito ◽  
Koji Yamamoto
Keyword(s):  
Growth Factor ◽  
Protein C ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Transforming Growth Factor Β ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

SummaryProtein C is a precursor of the anticoagulant serine protease, activated protein C, which inhibits coagulation factors Va and VIIIa. Although the liver appears to be the primary site of protein C synthesis, we previously demonstrated that the kidney and male reproductive organs also expressed abundant protein C mRNA in the mouse. In the present study, we further investigated the effects of tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), and transforming growth factor-β (TGF-β) on the expression of protein C mRNA in the principal producing organs, i.e., the liver, kidney, and testis. Both quantitative reverse transcription-PCR assay and in situ hybridization analysis revealed that TNF-α decreased protein C mRNA expression in the liver, kidney, and testis. IL-1 also down-regulated protein C mRNA expression in the liver and testis, but not in the kidney. In contrast, TGF-β unchanged the expression level of protein C mRNA in these three organs. These observations suggest that TNF-α and IL-1 may contribute to an increase in the procoagulant potential by down-regulation of protein C synthesis in the tissues during inflammatory processes.

Activated Protein C Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-α Production by Inhibiting Activation of both Nuclear Factor-κB and Activator Protein-1 in Human Monocytes

2002 ◽  
Vol 88 (08) ◽  
pp. 267-273 ◽  
Author(s):  
Mehtap Yuksel ◽  
Mitsuhiro Uchiba ◽  
Seikoh Horiuchi ◽  
Hiroaki Okabe ◽  
Kenji Okajima
Keyword(s):  
Protein C ◽  
Tumor Necrosis ◽  
Activated Protein C ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Activator Protein 1 ◽  
Tnf Α ◽  
Target Sites ◽  
Factor Α ◽  
Necrosis Factor

SummaryActivated protein C (APC), an important natural anticoagulant, inhibits tumor necrosis factor-α (TNF-α) production and attenuates various deleterious events induced by lipopolysaccharide (LPS), contributing thereby to a significant reduction of mortality in patients with severe sepsis. In this study, we investigated the mechanism(s) by which APC inhibits TNF-α production by LPS-stimulated human monocytes in vitro. Although APC inhibited LPS-induced TNF-α production in a concentration-dependent fashion, diisopropyl fluorophosphate-treated APC, an active-site-blocked APC, had no effect. APC inhibited both the binding of nuclear factor-κB (NF-κB) to target sites and the degradation of IκBα. APC also inhibited both the binding of activator protein-1 (AP-1) to target sites and the activation of mitogen-activated protein kinase pathways. These observations strongly suggest that APC inhibited LPS-induced TNF-α production by inhibiting the activation of both NF-κB and AP-1 and that the inhibitory activity of APC might depend on its serine protease activity. These results would at least partly explain the mechanism(s) by which APC reduces the tissue injury seen in animal models of sepsis and in patients with sepsis.

β-Carotene Concentration and Its Association with Inflammatory Biomarkers in Spanish Schoolchildren

2017 ◽  
Vol 71 (1-2) ◽  
pp. 80-87 ◽  
Author(s):  
Elena Rodríguez-Rodríguez ◽  
Ana M. López-Sobaler ◽  
Beatriz Navia ◽  
Pedro Andrés ◽  
Ana I. Jiménez-Ortega ◽  
...  
Keyword(s):  
High Sensitivity ◽  
Inflammatory Biomarkers ◽  
Reactive Protein ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Hs Crp ◽  
Α Level ◽  
Factor Α ◽  
Β Carotene ◽  
Necrosis Factor

Aim: To examine the correlation between inflammatory biomarkers and plasma β-carotene levels in children. Methods: A total of 564 Spanish schoolchildren aged 9-12 were observed and studied. Plasma β-carotene levels were assessed by HPLC. A β-carotene level <4.83 µg/dL (0.09 µmol/L) was considered deficient. Plasma tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by immunoenzyme assays. Serum high-sensitivity C-reactive protein (hs-CRP) was tested by immunonephelometry. Results: Subjects who were β-carotene-deficient (23.1% of the studied children) had higher IL-6 levels than subjects with normal β-carotene concentrations. The log-IL-6 and log-hs-CRP concentrations, but not the log-TNF-α level, were strongly and inversely related to the plasma log-β-carotene level (taking into account log-age, energy intake, log-triglycerides, gender, log-body mass index, log-β-carotene intake, energy from lipids and cholesterol as covariables). When the 3 inflammatory biomarkers were introduced into the regression model along with the corresponding covariables, only the log-IL-6 level was related to the plasma log-β-carotene level (β = -0.505 ± 0.078; p < 0.001). Conclusions: Inflammatory status, in particular IL-6 levels, appears to be negatively associated with plasma β-carotene levels in schoolchildren.

scholarly journals Attenuation of Oxidative Stress and Inflammation by Portulaca oleracea in Streptozotocin-Induced Diabetic Rats

2017 ◽  
Vol 22 (4) ◽  
pp. 562-566 ◽  
Author(s):  
Saeed Samarghandian ◽  
Abasalt Borji ◽  
Tahereh Farkhondeh
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Status ◽  
Total Antioxidant Status ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Portulaca Oleracea ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Factor Α ◽  
Necrosis Factor

The present study was designed to investigate the protective effect of the aqueous extract of Portulaca oleracea against hyperglycemic, oxidative damage and inflammation in the serum of streptozotocin (STZ)-induced diabetic rats. In the present study, the rats were divided into the following groups of 8 animals each: control, untreated diabetic, 3 Portulaca oleracea (100, 200, 400 mg/kg/d)–treated diabetic groups. At the end of the 4-week period, glucose, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), glutathione (GSH), and total antioxidant status (TAS) levels were measured. STZ caused an elevation in the serum levels of glucose, MDA, IL-6, and TNF-α with reduction in the levels of GSH and TAS ( P < .01). Portulaca oleracea ameliorated glucose, MDA, IL-6, TNF-α, GSH, and TAS levels in diabetic groups versus to the untreated groups ( P < .05). Taken together, Portulaca oleracea prevented hyperglycemia by preventing the oxidative stress and inflammation.

scholarly journals Longevity-Associated Variant of BPIFB4 Mitigates Monocyte-Mediated Acquired Immune Response

2019 ◽  
Vol 74 (Supplement_1) ◽  
pp. S38-S44 ◽  
Author(s):  
Elena Ciaglia ◽  
Francesco Montella ◽  
Anna Maciag ◽  
Pasqualina Scala ◽  
Anna Ferrario ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Therapeutic Potential ◽  
Human Monocyte ◽  
Peripheral Blood Mononuclear ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Cytokine Tumor Necrosis Factor ◽  
Pkc Alpha ◽  
Factor Α ◽  
Necrosis Factor

Abstract One of the basis of exceptional longevity is the maintaining of the balance between inflammatory and anti-inflammatory networks. The monocyte-macrophages activation plays a major role in tuning the immune responses, by oscillating between patrolling-protective to inflammatory status. Longevity-associated variant (LAV) of bactericidal/permeability-increasing fold-containing family B member 4 (BPIFB4) activates calcium, PKC-alpha, and eNOS, rescuing endothelial dysfunction in aged mice and inducing revascularization. The BPIFB4’s increment in serum of healthy long-living individuals (LLIs) compared to nonhealthy ones, its therapeutic potential in improving vascular homeostasis, which depends on immune system, together with its expression in bone marrow myeloid cells, suggests that LAV-BPIFB4 may improve immune regulation. Here we show that human monocytes exposed to LAV-BPIFB4 protein increased co-stimulatory molecules in resting state and reduced pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) after activating stimuli. Accordingly, a low percentage of CD69+ activated lymphocytes are found among LAV-BPIFB4-treated peripheral blood mononuclear cells (PBMCs). Moreover, human monocyte-derived dendritic cells (DCs) generated in presence of LAV-BPIFB4 secreted higher anti-(IL-10 and TGF-β) and lower pro-inflammatory (TNF-α and IL-1β) cytokines. Accordingly, LLIs’ plasma showed higher levels of circulating IL-10 and of neutralizing IL-1 receptor antagonist (IL-1RA) compared to controls. Thus, LAV-BPIFB4 effects on myeloid compartment could represent one example of a genetic predisposition carried by LLIs to protect from immunological dysfunctions.

Expression of Protein S in the Murine Heart and Cultured Mouse Cardiomyocytes Is Down-regulated by Cytokines

2001 ◽  
Vol 86 (08) ◽  
pp. 623-629 ◽  
Author(s):  
Takayoshi Shimokawa ◽  
Eriko Yamafuji ◽  
Tetsuhito Kojima ◽  
Hidehiko Saito ◽  
Koji Yamamoto
Keyword(s):  
Protein C ◽  
Interleukin 1 ◽  
Activated Protein C ◽  
Protein S ◽  
Suppressive Effect ◽  
Inflammatory Conditions ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

SummaryProtein S (PS), a co-factor of activated protein C, is a vitamin K-dependent anticoagulant protein and is known to be produced extrahepatically. In the present study, the concentration of PS mRNA was determined tissue by tissue in the mouse, and it was high in lung, adrenal and heart as well as in liver. We further investigated the effects of lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α), and interleukin-1 (IL-1) on the PS mRNA expression in murine tissues in vivo. Although LPS and TNF-α significantly decreased the expression level of PS mRNA in all tissues examined (e.g., lung, liver, heart, and kidney) and the PS antigen level in plasma, the suppressive effect of IL-1 on PS gene expression was limited to heart. More specifically, considerable amounts of PS mRNA and antigen were expressed in a cultured mouse cardiomyocyte cell line, and again, treatment with IL-1 decreased the PS expression in these cells. These observations raise a possibility that the expression of cardiac PS may contribute to the regional anticoagulant potential in heart, and suggest that the decreased PS expression by cytokines may result in an increase in the systemic and/or regional prothrombotic potential under inflammatory conditions.

Effect of Etanercept on Insulin Sensitivity in Nine Patients with Psoriasis

2007 ◽  
Vol 20 (4) ◽  
pp. 731-736 ◽  
Author(s):  
M. Marra ◽  
A. Campanati ◽  
R. Testa ◽  
C. Sirolla ◽  
A.R. Bonfigli ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Plasma Levels ◽  
Low Grade ◽  
Model Assessment ◽  
Plaque Type ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Factor Α ◽  
Low Grade Inflammation ◽  
Necrosis Factor

Metabolic syndrome is associated to chronic low grade inflammation, characterized by increased levels of inflammatory cytokines, such as Tumor Necrosis Factor-α (TNF-α) and Interleukin-6 (IL-6). In particular, TNF-α causes a decrease in the insulin-stimulated kinases related to the early phases of the insulin cascade, thereby leading to insulin resistance. Etanercept is a human fusion protein used in the treatment of psoriasis and inflammatory arthritis. It blocks inflammatory response by interfering in the binding of TNF-α to its receptors. The aim of this case report study is to verify the effect of Etanercept on insulin sensitivity, lipid profile and inflammatory status in psoriatic patients. Nine psoriatic patients with stable, active, plaque type psoriasis were enrolled and treated with Etanercept for 24 weeks. We found an improvement in the metabolic assessment with a significant reduction of insulin plasma levels. In particular, this treatment allows to maintain their euglycemic state with lower insulin plasma levels, as confirmed by the improved Homeostasis Model Assessment (HOMA) index. We conclude that Etanercept, probably acting on inflammation, improves insulin sensitivity in psoriatic subjects.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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