scholarly journals Effects of Palm Oil Tocotrienol-Rich Fraction (TRF) and Carotenes in Ovalbumin (OVA)-Challenged Asthmatic Brown Norway Rats

2019 ◽  
Vol 20 (7) ◽  
pp. 1764 ◽  
Author(s):  
Zaida Zainal ◽  
Afiqah Abdul Rahim ◽  
Huzwah Khaza’ai ◽  
Sui Kiat Chang
Keyword(s):  
Palm Oil ◽  
Time Course ◽  
Inflammatory Marker ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Rat Plasma ◽  
Brown Norway ◽  
Therapeutic Drugs ◽  
Potential Benefits ◽  
Norway Rats

Synthetic therapeutic drugs for asthma, a chronic airway inflammation characterised by strong eosinophil, mast cell, and lymphocyte infiltration, mucus hyper-production, and airway hyper-responsiveness, exhibit numerous side effects. Alternatively, the high antioxidant potential of palm oil phytonutrients, including vitamin E (tocotrienol-rich fractions; TRF) and carotene, may be beneficial for alleviating asthma. Here, we determined the therapeutic efficacy of TRF, carotene, and dexamethasone in ovalbumin-challenged allergic asthma in Brown Norway rats. Asthmatic symptoms fully developed within 8 days after the second sensitization, and were preserved throughout the time course via intranasal ovalbumin re-challenge. Asthmatic rats were then orally administered 30 mg/kg body weight TRF or carotene. TRF-treated animals exhibited reduced inflammatory cells in bronchial alveolar lavage fluid. TRF- and carotene-treated rats exhibited notable white blood cell reduction comparable to that from dexamethasone. TRF- and carotene-treatment also downregulated pro-inflammatory markers (IL-β, IL-6, TNF-α), coincident with anti-inflammatory marker IL-4 and IL-13 upregulation. Treatment significantly reduced asthmatic rat plasma CRP and IgE, signifying improved systemic inflammation. Asthmatic lung histology displayed severe edema and inflammatory cell infiltration in the bronchial wall, whereas treated animals retained healthy, normal-appearing lungs. The phytonutrients tocotrienol and carotene thus exhibit potential benefits for consumption as nutritional adjuncts in asthmatic disease.

scholarly journals Airway inflammatory cell responses to intra-amniotic lipopolysaccharide in a sheep model of chorioamnionitis

2009 ◽  
Vol 296 (3) ◽  
pp. L384-L393 ◽  
Author(s):  
Fook-Choe Cheah ◽  
J. Jane Pillow ◽  
Boris W. Kramer ◽  
Graeme R. Polglase ◽  
Ilias Nitsos ◽  
...  
Keyword(s):  
Time Course ◽  
Fetal Lung ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Protein Carbonyls ◽  
Sheep Model ◽  
Fetal Sheep ◽  
Nitrative Stress ◽  
Maturation Factor ◽  
Oxidative Burst Activity

Chorioamnionitis, a risk factor for bronchopulmonary dysplasia in preterm infants, causes an influx of inflammatory cells into the fetal lung. Using a fetal sheep model, we evaluated the time course of activation, functional maturity, and apoptosis of the leukocytes recruited to the fetal air spaces by lipopolysaccharide (LPS). Time-mated sheep were given intra-amniotic injections with 10 mg of Escherichia coli LPS or saline 2 or 7 days before preterm delivery at 124 days of gestation (term is 150 days). Both neutrophils and monocytes in bronchoalveolar lavage fluid (BALF) had activated NF-κB after 2- and 7-day LPS exposures. These neutrophils and monocytes expressed the activation factor CD11b and the maturation factor PU.1 at 2 days, and increased PU.1 expression was detected in macrophages at 7 days. Leukocyte oxidative burst activity was greatest at 7 days. BALF lipid peroxidation increased fivefold at 2 days, while protein carbonyls increased eightfold at 7 days. Nitrative stress was not detected in the BALF, but leukocytes in the lung expressed nitric oxide synthase (NOS)II (inducible NOS). BALF leukocytes expressed the antioxidant peroxiredoxin V. Lung glutathione peroxidase was also increased with LPS exposure. There was minimal apoptosis of airway and lung leukocytes assessed by caspase-3 activation. Intra-amniotic LPS recruits leukocytes to the fetal air space that have a persistent activation. These results have implications for the pathogenesis of lung inflammatory disorders in the preterm.

Reduction of allergic airway eosinophilia by dietary raffinose in Brown Norway rats

2004 ◽  
Vol 92 (2) ◽  
pp. 247-255 ◽  
Author(s):  
Hiroshi Watanabe ◽  
Kei Sonoyama ◽  
Jun Watanabe ◽  
Natsu Yamaguchi ◽  
Hiroto Kikuchi ◽  
...  
Keyword(s):  
Human Subjects ◽  
Control Diet ◽  
Disease Model ◽  
Intraperitoneal Administration ◽  
Lavage Fluid ◽  
Brown Norway ◽  
Intragastric Administration ◽  
Mrna Levels ◽  
Airway Eosinophilia ◽  
Norway Rats

Oral administration of raffinose, a naturally occurring indigestible oligosaccharide, has reportedly ameliorated atopic dermatitis in human subjects although the mechanism is unknown. The present study investigated the effect of dietary raffinose on allergen-induced airway eosinophilia in ovalbumin-sensitised Brown Norway rats as an atopic disease model. Brown Norway rats were immunised by subcutaneous injection with ovalbumin on day 0 and fed either a control diet or the diet supplemented with raffinose (50 g/kg diet). The rats were exposed to aerosolised ovalbumin on day 20, and broncho-alveolar lavage fluid was obtained on the next day. The number of eosinophils in the fluid was significantly lower in the rats fed the raffinose diet than in those fed the control diet. Dietary raffinose significantly reduced IL-4 and IL-5 mRNA levels in lung tissue and tended to lower ovalbumin-specific Ig E levels. Suppression of eosinophilia by dietary raffinose was still observed in caecectomised and neomycin-administered rats, suggesting little contribution by the colonic bacteria to the effect of raffinose. Intraperitoneal administration of raffinose also suppressed eosinophilia. Significant concentrations of raffinose were detected in portal venous and abdominal arterial plasma after the intragastric administration of raffinose. Overall, the findings suggest that dietary raffinose ameliorates allergic airway eosinophilia at least partly via post-absorptive mechanisms in Brown Norway rats.

Purification and characterization of plasma T-kininogen from Wistar and brown Norway rats

1989 ◽  
Vol 67 (2-3) ◽  
pp. 86-92 ◽  
Author(s):  
Albert Adam ◽  
Jacques Damas ◽  
Claire Renard ◽  
Germain Calay ◽  
Victor Bourdon
Keyword(s):  
Amino Acid ◽  
Cysteine Proteinase ◽  
Sugar Content ◽  
Gel Filtration ◽  
Rat Plasma ◽  
Brown Norway ◽  
Cysteine Proteinase Inhibitor ◽  
Neutral Sugar ◽  
Norway Rat ◽  
Norway Rats

A rapid and convenient three-step purification scheme has been developed for the purification of T-kininogen (alpha1-cysteine proteinase inhibitor) from rat plasma. The purification process includes chromatography on hydroxyapatite, immunoaffinity chromatography and gel filtration. This procedure is applied to plasma from the brown Norway rat which is known to be deficient in high and low molecular weight kininogens. The method furnished large amounts of T-kininogen from turpentine-treated Wistar rats as well as from untreated and turpentine-treated deficient brown Norway rats. The amino acid and hexose content of the three T-kininogens has been determined. While the composition of the molecules isolated from both injured rats was similar, the neutral sugar content of T-kininogen purified from untreated brown Norway rats was lower and its amino acid composition showed slight differences. The three molecules have identical behaviour and similar physicochemical and immunological properties when analysed by SDS electrophoresis, isoelectrofocusing and two-dimensional immunoelectrophoresis.Key words: T-kininogen, T-kinin, kallikrein–kininogen system.

scholarly journals Development and Characterization of an Allergic Asthma Rat Model for Interventional Studies

2020 ◽  
Vol 21 (11) ◽  
pp. 3841 ◽  
Author(s):  
Marta Périz ◽  
Francisco J. Pérez-Cano ◽  
Maria J. Rodríguez-Lagunas ◽  
Trinitat Cambras ◽  
Santiago Pastor-Soplin ◽  
...  
Keyword(s):  
Body Temperature ◽  
Allergic Asthma ◽  
Rat Model ◽  
Lavage Fluid ◽  
Brown Norway ◽  
Bordetella Pertussis Toxin ◽  
Objective Model ◽  
Norway Rats ◽  
Anaphylactic Response

Allergic asthma is one of the most common chronic diseases of the airways, however it still remains underdiagnosed and hence undertreated. Therefore, an allergic asthma rat model would be useful to be applied in future therapeutic strategy studies. The aim of the present study was to develop an objective model of allergic asthma in atopic rats that allows the induction and quantification of anaphylactic shock with quantitative variables. Female Brown Norway rats were intraperitoneally sensitized with ovalbumin (OVA), alum and Bordetella pertussis toxin and boosted a week later with OVA in alum. At day 28, all rats received an intranasal challenge with OVA. Anaphylactic response was accurately assessed by changes in motor activity and body temperature. Leukotriene concentration was determined in the bronchoalveolar lavage fluid (BALF), and total and IgE anti-OVA antibodies were quantified in blood and BALF samples. The asthmatic animals’ motility and body temperature were reduced after the shock for at least 20 h. The asthmatic animals developed anti-OVA IgE antibodies both in BALF and in serum. These results show an effective and relatively rapid model of allergic asthma in female Brown Norway rats that allows the quantification of the anaphylactic response.

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