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Folia Biol (Krakow) ; 64(3): 205-212, 2016.
Article in English | MEDLINE | ID: mdl-29847081

ABSTRACT

The study was performed to examine the actions of glucocorticoids on cytokine (TNF-α and IL-6) concentrations in blood plasma, adipose tissue and cytokines gene expression during acute (streptozotocin, STZ treatment) and chronic inflammation (overweight) in Swiss mice. The experiment was carried out on 6-week-old animals divided into two groups: I - non-obese (fed with a commercial food) and II - overweight mice (fed with a high-fat diet). In each group mice were divided into 4 experimental subgroups: I - control, II - acute inflammation (STZ), III - treated with glucocorticoids (DEX), and IV - STZ with DEX. After injections the animals were decapitated, blood and white adipose tissue (WAT) was quickly removed and directed to measure the plasma levels, tissue concentrations and gene expression of the cytokines (TNF-α, IL-6). Three weeks of treatment with a high-fat diet resulted in increased body weight gain and plasma level of cytokines, whereas did not change TNF-c and IL-6 mRNA gene expression in control animals. STZ, administered once, changed the TNF-α & and IL-6 concentrations in a different manner according to the diet. The TNF-a and IL-6 actions in mice white adipose tissue are down-regulated after glucocorticoids treatment only in overweight animals. The obtained results suggest that glucocorticoids' effects on adipose tissue immune response, both in a pro- and an anti-inflammatory manner, depend on the nutritional status.


Subject(s)
Adipose Tissue/metabolism , Dexamethasone/pharmacology , Inflammation/drug therapy , Interleukin-6/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Diabetes Mellitus, Experimental/metabolism , Diet, High-Fat/adverse effects , Energy Intake , Female , Glucocorticoids/pharmacology , Inflammation/etiology , Inflammation/metabolism , Interleukin-6/genetics , Mice , Overweight/physiopathology , RNA, Messenger/genetics , RNA, Messenger/metabolism , Tumor Necrosis Factor-alpha/genetics
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