Abstract | OBJECTIVE: SUMMARY BACKGROUND DATA: METHODS: RESULTS: A decrease in cardiac function and an increase in IL-6 and iNOS gene expression were observed following T-H. Androstenediol treatment normalized cardiac function, increased PPAR-gamma DNA binding activity, attenuated IL-6 and iNOS gene expressions, and reduced plasma IL-6. Plasma 15-deoxy-Delta12, 14-prostaglandin J2 ( PGJ2, an endogenous PPAR-gamma agonist) levels were also increased in androstenediol-treated T-H rats, but these levels were lower than those observed in shams. Coadministration of PPAR-gamma antagonist along with androstenediol, however, prevented the androstenediol-mediated reduction in cardiac iNOS and IL-6 expressions and abolished the improvements in cardiac function. CONCLUSION: The androstenediol-mediated salutary effects on cardiac function following T-H appear to be mediated at least in part via PPAR-gamma activation, which down-regulates IL-6 and iNOS gene expression in the heart.
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Authors | Tomoharu Shimizu, László Szalay, Ya-Ching Hsieh, Takao Suzuki, Mashkoor A Choudhry, Kirby I Bland, Irshad H Chaudry |
Journal | Annals of surgery
(Ann Surg)
Vol. 244
Issue 1
Pg. 131-8
(Jul 2006)
ISSN: 0003-4932 [Print] United States |
PMID | 16794398
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- 2-chloro-5-nitrobenzanilide
- Anabolic Agents
- Anilides
- Interleukin-6
- PPAR gamma
- 9-deoxy-delta-9-prostaglandin D2
- Androstenediol
- Nitric Oxide Synthase Type II
- Prostaglandin D2
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Topics |
- Anabolic Agents
(pharmacology)
- Androstenediol
(pharmacology)
- Anilides
(pharmacology)
- Animals
- Blotting, Western
- Cardiac Output
(drug effects)
- Electrophoretic Mobility Shift Assay
- Gene Expression
- Interleukin-6
(blood, metabolism)
- Male
- Myocardium
(metabolism)
- Nitric Oxide Synthase Type II
(metabolism)
- PPAR gamma
(agonists, antagonists & inhibitors, metabolism)
- Prostaglandin D2
(analogs & derivatives, blood)
- Rats
- Rats, Sprague-Dawley
- Shock, Hemorrhagic
(metabolism, physiopathology)
- Ventricular Function, Left
(drug effects)
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