Glucocorticoid receptor antagonist RU 486 treatment reduces periodontitis in Fischer 344 rats

2000 ◽  
Vol 35 (5) ◽  
pp. 285-290 ◽  
Author(s):  
T. Breivik ◽  
P. S. Thrane ◽  
P. Gjermo ◽  
P. K. Opstad
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Fischer 344 Rats ◽  
Ru 486 ◽  
Fischer 344

Stress alters cutaneous permeability barrier homeostasis

2000 ◽  
Vol 278 (2) ◽  
pp. R367-R372 ◽  
Author(s):  
Mitsuhiro Denda ◽  
Toru Tsuchiya ◽  
Peter M. Elias ◽  
Kenneth R. Feingold
Keyword(s):  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Psychological Stress ◽  
Skin Disease ◽  
Barrier Function ◽  
Plasma Corticosterone ◽  
Permeability Barrier ◽  
Hairless Mice ◽  
Ru 486 ◽  
Kinetics Of

Recent studies have shown that psychological stress can influence cutaneous barrier function, suggesting that this form of stress could trigger or aggravate skin disease. In the present study, we demonstrate that transfer of hairless mice to a different cage delays barrier recovery rates. Pretreatment with a phenothiazine sedative, chlorpromazine, before transfer of animals restored the kinetics of barrier recovery toward normal, suggesting that psychological stress is the basis for this alteration in barrier homeostasis. To determine the mechanism linking psychological stress to altered barrier recovery, we first demonstrated that plasma corticosterone levels increase markedly after transfer of animals to new cages and that pretreatment with chlorpromazine blocks this increase. Second, we demonstrated that the systemic administration of corticosterone delays barrier recovery. Finally, we demonstrated that pretreatment with the glucocorticoid receptor antagonist RU-486 blocks the delay in barrier recovery produced by systemic corticosterone, change of cage, or immobilization. These results suggest that psychological stress stimulates increased production of glucocorticoids, which, in turn, adversely affects permeability barrier homeostasis.

Endogenous glucocorticoids released during acute toxic liver injury enhance hepatic IL-10 synthesis and release

1999 ◽  
Vol 276 (1) ◽  
pp. G199-G205 ◽  
Author(s):  
Mark G. Swain ◽  
Caroline Appleyard ◽  
John Wallace ◽  
Howard Wong ◽  
Tai Le
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Glucocorticoid Receptor ◽  
Receptor Antagonist ◽  
Mrna Expression ◽  
Elevated Serum ◽  
Ru 486 ◽  
Tnf Α ◽  
Toxic Liver Injury ◽  
Acute Toxic

Endogenous glucocorticoids are known to play a role in the regulation of the inflammatory response possibly by modulating pro- and anti-inflammatory cytokine expression. We examined endogenous glucocorticoid secretion, hepatic damage, tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) mRNA expression and release in rats treated with carbon tetrachloride (CCl4) after treatment with vehicle or a glucocorticoid receptor antagonist (RU-486). Rats treated with CCl4 demonstrated striking elevations of plasma corticosterone levels. Inhibition of endogenous glucocorticoid activity by pretreatment with the glucocorticoid receptor antagonist RU-486 resulted in augmented CCl4-mediated hepatotoxicity, as reflected by histology and serum transaminase levels, which were independent of alterations in serum TNF-α levels or hepatic mRNA expression. CCl4 treatment resulted in enhanced hepatic IL-10 mRNA expression and elevated serum IL-10 levels, which were markedly attenuated by glucocorticoid receptor blockade. In summary, significant endogenous glucocorticoid release occurs during acute toxic liver injury in the rat and suppresses the inflammatory response independent of effects on TNF-α but possibly by upregulating hepatic IL-10 production.

Characterization of the vulnerability to repeated stress in Fischer 344 rats: possible involvement of microRNA-mediated down-regulation of the glucocorticoid receptor

2008 ◽  
Vol 27 (9) ◽  
pp. 2250-2261 ◽  
Author(s):  
Shusaku Uchida ◽  
Akira Nishida ◽  
Kumiko Hara ◽  
Toshiki Kamemoto ◽  
Masatomo Suetsugi ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Fischer 344 Rats ◽  
Down Regulation ◽  
Fischer 344 ◽  
Repeated Stress

The effects of the selective 5-HT2C receptor antagonist SB 242084 on learned helplessness in male Fischer 344 rats

2008 ◽  
Vol 203 (4) ◽  
pp. 665-675 ◽  
Author(s):  
Paul V. Strong ◽  
Benjamin N. Greenwood ◽  
Monika Fleshner
Keyword(s):  
Receptor Antagonist ◽  
Learned Helplessness ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Sb 242084

Chronic Toxicity, Metabolism, and Pharmacokinetics of the 5-HT3 Receptor Antagonist Zatosetron (LY277359) in Fischer 344 Rats

1994 ◽  
Vol 22 (4) ◽  
pp. 494-504 ◽  
Author(s):  
ALISON M. BENDELE ◽  
DIANE A. BUENGER ◽  
JOHN P. MCGRATH ◽  
CHRIS A. SCHMALZ ◽  
GEORGE K. HANASONO
Keyword(s):  
Receptor Antagonist ◽  
Chronic Toxicity ◽  
Fischer 344 Rats ◽  
Fischer 344
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