Effect of white tea consumption on serum leptin, TNF-α and UCP1 gene expression in ovariectomized rats

Abstract The decrease in estrogen in menopausal women increases body fat. The present studies were undertaken to investigate the involvement of estrogen in leptin production in vivo. In the first study, expression of ob gene mRNA in white adipose tissue was measured at 2 and 8 weeks after ovariectomy in rats. In the second, serum leptin concentration was measured in total body fat of 87 weight-matched human subjects (29 men, 29 premenopausal and 29 postmenopausal women). In the third, changes in serum leptin concentration with the menstrual cycle were determined, ob gene expression decreased in subcutaneous and retroperitoneal white adipose tissue of ovariectomized rats 8 weeks after the operation, while ovariectomy increased ob gene expression in mesenteric white adipose tissue. Serum leptin concentration was decreased by ovariectomy. Estradiol supplement reversed the effect of ovariectomy on ob gene expression and circulating leptin levels. In humans, serum leptin concentration was higher in premenopausal women than in men, and in postmenopausal women it was lower than in premenopausal women, but still higher than in men. In 13 premenopausal women, serum leptin levels were significantly higher in the luteal phase than in the follicular phase. The present studies strongly indicate that estrogen regulates leptin production in rats and human subjects in vivo. Regional variation in the regulation of ob gene expression by estrogen was found. Journal of Endocrinology (1997) 154, 285–292

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TNF-α and IFN-γ-mediated signal transduction pathways: Effects on IRF-1 and MHC class I gene expression in oligodendrocytes

Immunology Letters ◽

10.1016/s0165-2478(97)88732-9 ◽

1997 ◽

Vol 56 (1-3) ◽

pp. 465

Author(s):

C Agresti

Keyword(s):

Gene Expression ◽

Signal Transduction ◽

Mhc Class I ◽

Class I ◽

Signal Transduction Pathways ◽

Tnf Α ◽

Ifn Γ ◽

I Gene ◽

Mhc Class I Gene

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PECAM–1 (CD31)-gene expression is downregulated by TNF-α or Interferon (IFN-) but upregulated by TGF–1 in peripheral blood leukocytes

Zeitschrift für Gastroenterologie ◽

10.1055/s-0031-1295864 ◽

2012 ◽

Vol 50 (01) ◽

Author(s):

F Moriconi ◽

A Amanzada ◽

I Malik ◽

G Ramadori

Keyword(s):

Gene Expression ◽

Peripheral Blood ◽

Peripheral Blood Leukocytes ◽

Blood Leukocytes ◽

Tnf Α

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Anti-Rheumatic Effect of Antisense Oligonucleotide Cytos-11 Targeting TNF-α Expression

International Journal of Molecular Sciences ◽

10.3390/ijms22031022 ◽

2021 ◽

Vol 22 (3) ◽

pp. 1022

Author(s):

Tatyana P. Makalish ◽

Ilya O. Golovkin ◽

Volodymyr V. Oberemok ◽

Kateryna V. Laikova ◽

Zenure Z. Temirova ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Gene Expression ◽

Rat Model ◽

Peripheral Blood ◽

Antisense Oligonucleotide ◽

Joint Inflammation ◽

Blood Concentrations ◽

Tnf Α ◽

Effective Drugs ◽

First Time

The urgency of the search for inexpensive and effective drugs with localized action for the treatment of rheumatoid arthritis continues unabated. In this study, for the first time we investigated the Cytos-11 antisense oligonucleotide suppression of TNF-α gene expression in a rat model of rheumatoid arthritis induced by complete Freund’s adjuvant. Cytos-11 has been shown to effectively reduce peripheral blood concentrations of TNF-α, reduce joint inflammation, and reduce pannus development. The results achieved following treatment with the antisense oligonucleotide Cytos-11 were similar to those of adalimumab (Humira®); they also compared favorably with those results, which provides evidence of the promise of drugs based on antisense technologies in the treatment of this disease.

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The impacts of an eight-week moderate aerobic exercise training on some gene expression involved in cholesterol metabolism in ovariectomized rats

Sport Sciences for Health ◽

10.1007/s11332-020-00701-y ◽

2021 ◽

Author(s):

Maryam Emamian Rostami ◽

Rozita Fathi ◽

Khadijeh Nasiri

Keyword(s):

Gene Expression ◽

Exercise Training ◽

Aerobic Exercise ◽

Cholesterol Metabolism ◽

Aerobic Exercise Training ◽

Ovariectomized Rats

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A Novel Method Facilitating the Simple and Low-Cost Preparation of Human Osteochondral Slice Explants for Large-Scale Native Tissue Analysis

International Journal of Molecular Sciences ◽

10.3390/ijms22126394 ◽

2021 ◽

Vol 22 (12) ◽

pp. 6394

Author(s):

Jacob Spinnen ◽

Lennard K. Shopperly ◽

Carsten Rendenbach ◽

Anja A. Kühl ◽

Ufuk Sentürk ◽

...

Keyword(s):

Gene Expression ◽

Cell Viability ◽

Large Scale ◽

Marker Gene ◽

Cell Swelling ◽

Tissue Cell ◽

Joint Research ◽

Sample Number ◽

Tnf Α ◽

Novel Method

For in vitro modeling of human joints, osteochondral explants represent an acceptable compromise between conventional cell culture and animal models. However, the scarcity of native human joint tissue poses a challenge for experiments requiring high numbers of samples and makes the method rather unsuitable for toxicity analyses and dosing studies. To scale their application, we developed a novel method that allows the preparation of up to 100 explant cultures from a single human sample with a simple setup. Explants were cultured for 21 days, stimulated with TNF-α or TGF-β3, and analyzed for cell viability, gene expression and histological changes. Tissue cell viability remained stable at >90% for three weeks. Proteoglycan levels and gene expression of COL2A1, ACAN and COMP were maintained for 14 days before decreasing. TNF-α and TGF-β3 caused dose-dependent changes in cartilage marker gene expression as early as 7 days. Histologically, cultures under TNF-α stimulation showed a 32% reduction in proteoglycans, detachment of collagen fibers and cell swelling after 7 days. In conclusion, thin osteochondral slice cultures behaved analogously to conventional punch explants despite cell stress exerted during fabrication. In pharmacological testing, both the shorter diffusion distance and the lack of need for serum in the culture suggest a positive effect on sensitivity. The ease of fabrication and the scalability of the sample number make this manufacturing method a promising platform for large-scale preclinical testing in joint research.

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Modulatory Effects of Osthole on Lipopolysaccharides-Induced Inflammation in Caco-2 Cell Monolayer and Co-Cultures with THP-1 and THP-1-Derived Macrophages

Nutrients ◽

10.3390/nu13010123 ◽

2020 ◽

Vol 13 (1) ◽

pp. 123

Author(s):

Natalia K. Kordulewska ◽

Justyna Topa ◽

Małgorzata Tańska ◽

Anna Cieślińska ◽

Ewa Fiedorowicz ◽

...

Keyword(s):

Gene Expression ◽

Inflammatory Reaction ◽

Wide Spectrum ◽

Cell Monolayer ◽

In Vivo Studies ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Tnf Α

Lipopolysaccharydes (LPS) are responsible for the intestinal inflammatory reaction, as they may disrupt tight junctions and induce cytokines (CKs) secretion. Osthole has a wide spectrum of pharmacological effects, thus its anti-inflammatory potential in the LPS-treated Caco-2 cell line as well as in Caco-2/THP-1 and Caco-2/macrophages co-cultures was investigated. In brief, Caco-2 cells and co-cultures were incubated with LPS to induce an inflammatory reaction, after which osthole (150–450 ng/mL) was applied to reduce this effect. After 24 h, the level of secreted CKs and changes in gene expression were examined. LPS significantly increased the levels of IL-1β, -6, -8, and TNF-α, while osthole reduced this effect in a concentration-dependent manner, with the most significant decrease when a 450 ng/mL dose was applied (p < 0.0001). A similar trend was observed in changes in gene expression, with the significant osthole efficiency at a concentration of 450 ng/μL for IL1R1 and COX-2 (p < 0.01) and 300 ng/μL for NF-κB (p < 0.001). Osthole increased Caco-2 monolayer permeability, thus if it would ever be considered as a potential drug for minimizing intestinal inflammatory symptoms, its safety should be confirmed in extended in vitro and in vivo studies.

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LPS-induced expression of CD14 in the TRIF pathway is epigenetically regulated by sulforaphane in porcine pulmonary alveolar macrophages

Innate Immunity ◽

10.1177/1753425916669418 ◽

2016 ◽

Vol 22 (8) ◽

pp. 682-695 ◽

Cited By ~ 12

Author(s):

Qin Yang ◽

Maren J Pröll ◽

Dessie Salilew-Wondim ◽

Rui Zhang ◽

Dawit Tesfaye ◽

...

Keyword(s):

Gene Expression ◽

Alveolar Macrophages ◽

Methylation Status ◽

Gene Body ◽

Gene Body Methylation ◽

Tnf Α ◽

Pulmonary Alveolar Macrophages ◽

Cluster Of Differentiation ◽

Cd14 Gene

Pulmonary alveolar macrophages (AMs) are important in defense against bacterial lung inflammation. Cluster of differentiation 14 (CD14) is involved in recognizing bacterial lipopolysaccharide (LPS) through MyD88-dependent and TRIF pathways of innate immunity. Sulforaphane (SFN) shows anti-inflammatory activity and suppresses DNA methylation. To identify CD14 epigenetic changes by SFN in the LPS-induced TRIF pathway, an AMs model was investigated in vitro. CD14 gene expression was induced by 5 µg/ml LPS at the time point of 12 h and suppressed by 5 µM SFN. After 12 h of LPS stimulation, gene expression was significantly up-regulated, including TRIF, TRAF6, NF-κB, TRAF3, IRF7, TNF-α, IL-1β, IL-6, and IFN-β. LPS-induced TRAM, TRIF, RIPK1, TRAF3, TNF-α, IL-1β and IFN-β were suppressed by 5 µM SFN. Similarly, DNMT3a expression was increased by LPS but significantly down-regulated by 5 µM SFN. It showed positive correlation of CD14 gene body methylation with in LPS-stimulated AMs, and this methylation status was inhibited by SFN. This study suggests that SFN suppresses CD14 activation in bacterial inflammation through epigenetic regulation of CD14 gene body methylation associated with DNMT3a. The results provide insights into SFN-mediated epigenetic down-regulation of CD14 in LPS-induced TRIF pathway inflammation and may lead to new methods for controlling LPS-induced inflammation in pigs.

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