scholarly journals Effects of oral administration of essential oils on anti-immune stress, antimicrobial properties, and repairing the intestinal damage in broilers challenged by lipopolysaccharide

2019 ◽  
Vol 99 (2) ◽  
pp. 377-383
Author(s):  
S.D. Liu ◽  
M.H. Song ◽  
W. Yun ◽  
J.H. Lee ◽  
H.B. Kim ◽  
...  
Keyword(s):  
Oral Administration ◽  
Essential Oils ◽  
Antimicrobial Properties ◽  
Basal Diet ◽  
Intestinal Damage ◽  
Abnormal Growth ◽  
Immune Stress ◽  
Factor Α ◽  
Necrosis Factor

The aim of the present study was to evaluate the effects of oral administration of essential oils (carvacrol, thyme, and oregano) on anti-immune stress, antimicrobial properties, and repairing the intestinal damage caused by Salmonella enterica lipopolysaccharides (LPS) in broilers. A total of 100 Ross 308 broilers (21-d-old; 1.10 ± 0.11 kg) were randomly allocated to five groups: T1, basal diet + saline; T2, basal diet + LPS; T3, basal diet + 200 μL carvacrol oils + LPS; T4, basal diet + 200 μL thyme oils + LPS; T5, basal diet + 200 μL oregano oils + LPS, with 20 replicates each, and one chicken per replicate per cage. Those challenged by LPS resulted in an immune stress, which manifests as the abnormal growth (P < 0.05) in immune organs, and the content of immunoglobulin G (P < 0.05), tumor necrosis factor-α (P < 0.05), and the rectum temperature (P < 0.05) increased compared with other groups. The oral administration of essential oils controlled the immune stress to a certain extent. The essential oils could reduce harmful bacteria, such as Escherichia coli (P < 0.05) and Salmonella enumeration (P < 0.05), in vivo of broilers. Meanwhile, the essential oils repaired the intestinal damage, which showed a reduction in the villi height (P < 0.05) and goblet cell (P < 0.05) caused by LPS. In conclusion, the essential oils (carvacrol, thyme, and oregano essential oils) controlled the stress reaction and maintained intestinal health to a certain extent.

scholarly journals PSVII-3 Effects of oral administration of essential oils on anti-immune stress, antimicrobial and repairing the intestinal damage in broilers challenged by lipopolysaccharide

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 171-171
Author(s):  
Hanjin Oh ◽  
Shudong Liu ◽  
Won Yun ◽  
Jihwan Lee ◽  
Jiseon An ◽  
...  
Keyword(s):  
Oral Administration ◽  
Essential Oils ◽  
Basal Diet ◽  
Stress Reaction ◽  
Intestinal Damage ◽  
E Coli ◽  
Abnormal Growth ◽  
Immune Stress ◽  
Tnf Α

Abstract The aim of the present study was to evaluate the effects of oral administration of essential oils (Carvacrol, Thyme and Oregano essential oils) on anti-immune stress, antimicrobial and repairing the intestinal damage, caused by Salmonella enterica Lipopolysaccharide, in vivo of broilers. A total of 100 ROSS 308 broilers (21-day-old; 1.10 ± 0.11kg) were randomly allocated to 5 groups, T1: basal diet + Saline; T2: basal diet + LPS; T3: basal diet+ 200μL carvacrol oils+ LPS; T4: basal diet+ 200μL thyme oils+ LPS; T5: basal diet+ 200μL oregano oils+ LPS, with 20 replicates every group, and 1 chicken per replicate per cage. The challenged by LPS resulted in an immune stress, which manifests as the abnormal growth (P < 0.05) in immune organs, the content of IgG (P < 0.05) and TNF-α(P < 0.05) and the rectum temperature (P < 0.05) increased compared with other groups; the oral administration of essential oils controlled the immune stress to a certain extent. The essential oils could withhold maleficent bacteria, as E. coli (P < 0.05) and Salmonella enumeration (P < 0.05), in vivo of the broiler. Meanwhile, the essential oils repaired the intestinal damage which shown a reduction in the villi height (P < 0.05) and goblet cell (P < 0.05) caused by LPS. In conclusion, the essential oils (Carvacrol, Thyme and Oregano essential oils) controlled the stress reaction and maintain intestinal health to a certain extent. http://www.conferenceharvester.com/

Synthesis of 8-alkoxy-1,3-dimethyl-2, 6-dioxopurin-7-yl-substituted acetohydrazides and butanehydrazides as analgesic and anti-inflammatory agents

2015 ◽  
Vol 21 (5) ◽  
pp. 273-278 ◽  
Author(s):  
Grażyna Chłoń-Rzepa ◽  
Agnieszka W. Jankowska ◽  
Małgorzata Zygmunt ◽  
Krzysztof Pociecha ◽  
Elżbieta Wyska
Keyword(s):  
Analgesic Activity ◽  
Structural Element ◽  
Hot Plate ◽  
Hot Plate Test ◽  
Peripheral Mechanism ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor ◽  
Inhibit Tumor Necrosis Factor

AbstractA series of new 8-alkoxy-1,3-dimethyl-2,6-dioxopurin-7-yl-substituted acetohydrazides and butanehydrazides 6–12 was synthesized and evaluated for the analgesic activity in two in vivo models: the writhing syndrome and the hot-plate tests. Among the investigated derivatives, compounds with N′-arylidenehydrazide moiety 9–12 show analgesic activity significantly higher than that of acetylsalicylic acid, which may indicate the importance of this structural element for analgesic properties. The lack of the activity in the hot-plate test may suggest that the analgesic activity of the newly synthesized compounds is mediated by a peripheral mechanism. The selected compounds 7 and 12 inhibit tumor necrosis factor α production in a rat model of lipopolysaccharide-induced endotoxemia, similarly to theophylline, which may confirm their anti-inflammatory properties.

scholarly journals In Vivo and in Vitro Evidence for the Involvement of Tumor Necrosis Factor-α in the Induction of Leptin by Lipopolysaccharide*

Endocrinology ◽  
1998 ◽  
Vol 139 (5) ◽  
pp. 2278-2283 ◽  
Author(s):  
Brian N. Finck ◽  
Keith W. Kelley ◽  
Robert Dantzer ◽  
Rodney W. Johnson
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Repetitive Injections of Dendritic Cells Matured with Tumor Necrosis Factor α Induce Antigen-specific Protection of Mice from Autoimmunity

2001 ◽  
Vol 195 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Mauritius Menges ◽  
Susanne Rößner ◽  
Constanze Voigtländer ◽  
Heike Schindler ◽  
Nicole A. Kukutsch ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Cell Immunity ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Mature dendritic cells (DCs) are believed to induce T cell immunity, whereas immature DCs induce T cell tolerance. Here we describe that injections of DCs matured with tumor necrosis factor (TNF)-α (TNF/DCs) induce antigen-specific protection from experimental autoimmune encephalomyelitis (EAE) in mice. Maturation by TNF-α induced high levels of major histocompatibility complex class II and costimulatory molecules on DCs, but they remained weak producers of proinflammatory cytokines. One injection of such TNF/DCs pulsed with auto-antigenic peptide ameliorated the disease score of EAE. This could not be observed with immature DCs or DCs matured with lipopolysaccharide (LPS) plus anti-CD40. Three consecutive injections of peptide-pulsed TNF/DCs derived from wild-type led to the induction of peptide-specific predominantly interleukin (IL)-10–producing CD4+ T cells and complete protection from EAE. Blocking of IL-10 in vivo could only partially restore the susceptibility to EAE, suggesting an important but not exclusive role of IL-10 for EAE prevention. Notably, the protection was peptide specific, as TNF/DCs pulsed with unrelated peptide could not prevent EAE. In conclusion, this study describes that stimulation by TNF-α results in incompletely matured DCs (semi-mature DCs) which induce peptide-specific IL-10–producing T cells in vivo and prevent EAE.

Nonstressed rat model of acute endotoxemia that unmasks the endotoxin-induced TNF-α response

1999 ◽  
Vol 276 (2) ◽  
pp. H671-H678 ◽  
Author(s):  
David W. A. Beno ◽  
Robert E. Kimura
Keyword(s):  
Rat Model ◽  
Endotoxic Shock ◽  
Stress Hormones ◽  
Tnf Α ◽  
Baseline Concentrations ◽  
Experimental Protocols ◽  
Factor Α ◽  
Necrosis Factor

Previous investigators have demonstrated that the tumor necrosis factor-α (TNF-α) response to endotoxin is inhibited by exogenous corticosterone or catecholamines both in vitro and in vivo, whereas others have reported that surgical and nonsurgical stress increase the endogenous concentrations of these stress-induced hormones. We hypothesized that elevated endogenous stress hormones resultant from experimental protocols attenuated the endotoxin-induced TNF-α response. We used a chronically catheterized rat model to demonstrate that the endotoxin-induced TNF-α response is 10- to 50-fold greater in nonstressed (NS) rats compared with either surgical-stressed (SS, laparotomy) or nonsurgical-stressed (NSS, tail vein injection) models. Compared with the NS group, the SS and NSS groups demonstrated significantly lower mean peak TNF-α responses at 2 mg/kg and 6 μg/kg endotoxin [NS 111.8 ± 6.5 ng/ml and 64.3 ± 5.9 ng/ml, respectively, vs. SS 3.9 ± 1.1 ng/ml ( P < 0.01) and 1.3 ± 0.5 ng/ml ( P < 0.01) or NSS 5.2 ± 3.2 ng/ml ( P < 0.01) at 6 μg/kg]. Similarly, baseline concentrations of corticosterone and catecholamines were significantly lower in the NSS group [84.5 ± 16.5 ng/ml and 199.8 ± 26.2 pg/ml, respectively, vs. SS group 257.2 ± 35.7 ng/ml ( P< 0.01) and 467.5 ± 52.2 pg/ml ( P < 0.01) or NS group 168.6 ± 14.4 ng/ml ( P < 0.01) and 1,109.9 ± 140.7 pg/ml ( P < 0.01)]. These findings suggest that the surgical and nonsurgical stress inherent in experimental protocols increases baseline stress hormones, masking the endotoxin-induced TNF-α response. Subsequent studies of endotoxic shock should control for the effects of protocol-induced stress and should measure and report baseline concentrations of corticosterone and catecholamines.

scholarly journals Evaluation In Vivo and In Vitro of the Antioxidant, Antinociceptive, and Anti-Inflammatory Activities of Biflavonoids From Ouratea hexasperma and O. ferruginea

2019 ◽  
Vol 14 (6) ◽  
pp. 1934578X1985680 ◽  
Author(s):  
Poliana de Araujo Oliveira ◽  
Queli Cristina Fidelis ◽  
Thayane Ferreira da Costa Fernandes ◽  
Milene Conceição de Souza ◽  
Dayane Magalhães Coutinho ◽  
...  
Keyword(s):  
Type I Collagen ◽  
In Vivo Model ◽  
Type I ◽  
Anti Inflammatory ◽  
Vitro Model ◽  
Factor Α ◽  
Necrosis Factor

Ouratea species are used for the treatment of inflammation-related diseases such as rheumatism and arthritic disorders. The Ouratea genus is a rich source of flavonoids and bioflavonoids and for this reason we evaluated the effects of the biflavonoid fractions from the leaves of O. hexasperma (OHME) and O. ferruginea (OFME) in the in vivo model of complete Freund’s adjuvant (CFA)-induced arthritis and in the in vitro model of oxidative stress and cellular viability. The CFA-induced arthritis model in rats was followed by paw volume, articular incapacitation and Randall-selitto models, as well as quantification of cytokines and serum C-terminal telopeptide of type I collagen levels. OHME and OFME demonstrated antinociceptive and anti-inflammatory activities, as well as improvement in articular incapacity and reduction in levels of interleukin 1β (IL-1β), IL-6, tumor necrosis factor α, and type 1 collagen, and increased cell viability. No adverse effects were observed. The results suggest that OHME and OFME can reduce inflammation and bone resorption besides their antioxidant action.

Estriol sensitizes rat Kupffer cells via gut-derived endotoxin

1999 ◽  
Vol 277 (3) ◽  
pp. G671-G677 ◽  
Author(s):  
Nobuyuki Enomoto ◽  
Shunhei Yamashina ◽  
Peter Schemmer ◽  
Chantal A. Rivera ◽  
Blair U. Bradford ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Kupffer Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Sublethal Dose ◽  
Intracellular Ca ◽  
Serum Transaminases ◽  
Factor Α ◽  
Necrosis Factor

The relationship between gender and alcohol-induced liver disease is complex; however, endotoxin is most likely involved. Recently, it was reported that estriol activated Kupffer cells by upregulation of the endotoxin receptor CD14. Therefore, the purpose of this work was to study how estriol sensitizes Kupffer cells. Rats were given estriol (20 mg/kg ip), and Kupffer cells were isolated 24 h later. After addition of lipopolysaccharide (LPS), intracellular Ca2+ concentration was measured using a microspectrofluorometer with the fluorescent indicator fura 2, and tumor necrosis factor-α was measured by ELISA. CD14 was evaluated by Western analysis. One-half of the rats given estriol intraperitoneally 24 h before an injection of a sublethal dose of LPS (5 mg/kg) died within 24 h, whereas none of the control rats died. Mortality was prevented totally by sterilization of the gut with antibiotics. A similar pattern was obtained with liver histology and serum transaminases. Translocation of horseradish peroxidase was increased about threefold in gut segments by treatment with estriol. This increase was not altered by treatment with nonabsorbable antibiotics. On the other hand, endotoxin levels were increased to 60–70 pg/ml in plasma of rats treated with estriol. As expected, this increase was prevented (<20 pg/ml) by antibiotics. In isolated Kupffer cells, LPS-induced increases in intracellular Ca2+ concentration, tumor necrosis factor-α production, and CD14 were increased, as previously reported. All these phenomena were blocked by antibiotics. Therefore, it is concluded that estriol treatment in vivo sensitizes Kupffer cells to LPS via mechanisms dependent on increases in CD14. This is most likely due to elevated portal blood endotoxin caused by increased gut permeability.

scholarly journals Short-term alpha- or gamma-delta-enriched tocopherol oil supplementation differentially affects the expression of proinflammatory mediators: selective impacts on characteristics of protein tyrosine nitration in vivo

2013 ◽  
Vol 3 (1) ◽  
pp. 6 ◽  
Author(s):  
Ted H. Elsasser ◽  
Stanislaw Kahl ◽  
Katie M. Lebold ◽  
Maret G. Traber ◽  
Jessica Shaffer ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Short Term ◽  
Proinflammatory Response ◽  
E Coli ◽  
Amyloid A ◽  
Proinflammatory Mediators ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

While vitamin E has been used for decades in cattle diets, the principle form used traditionally is the synthetic α-isoform acetate or succinate and largely no data exist on the biological partitioning or functionality of the major naturally occurring γ- and δ-isoforms in cattle. Using tyrosine 3’-nitrated protein (pNT) as a biomarker of nitrosative cell stress, we sought to evaluate the effectiveness of short-term feeding supplementation of high content natural α-tocopherol (<em>α-T</em>, 96% α-isomer) compared to high content γ- and δ-enriched low α-content mixed tocopherol oils (<em>γ-T</em>, ~70% <em>γ-</em>, 20% δ-, &lt;5% α-isoform) to mitigate systemic and hepatic aspects of the proinflammatory response to endotoxin (LPS). Calves fed diets supplemented with <em>α-T</em>, <em>γ-T</em> for five days or no tocopherol supplement (<em>T0E</em>) were challenged with a low-level of LPS (0.25 μg/kg, iv, <em>E. coli </em>055:B5) sufficient to effect a liver nitration response. As fed,<em> α-T</em> or <em>γ-T</em> increased plasma and liver content of the respective tocopherols reflecting their relative abundance in the respective diets. Plasma or tissue mediators and biomarkers of the proinflammatory response [plasma concentrations of tumor necrosis factor-α (TNF-α, P&lt;0.001), nitrate+nitrite (NOx, P&lt;0.01), and serum amyloid A (SAA, P&lt;0.001)], and general liver content of pNT (P&lt;0.005) increased after LPS. LPS-mediated increases in TNF-α were not dif- ferent between diet treatments; both plasma NOx (P&lt;0.05) and generalized liver pNT (P&lt;0.03) responses were attenuated significantly in <em>α-T </em>and <em>γ-T versus T0E calves</em>. Plasma SAA was significantly decreased in γ-T calves at 24 h post-LPS relative to responses in <em>α-T</em> or <em>T0E </em>calves. The nitration of the mitochondrial proteins 24 h post-LPS was not only attenuated in <em>α-T</em> and <em>γ-T vs T0E</em>, but also the mitigating effect of <em>γ-T</em> on these specific nitration events was greater than that of <em>α-T </em>(P&lt;0.01). Results are consistent with the concept that short-term <em>α-T</em> or <em>γ-T</em> supplementation can effectively decrease proinflammatory liver pNT after LPS; some mitochondrial nitration targets may be better protected with prophylactic supplementation with γ-,δ-tocopherol enriched oil.

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