A Role of PPAR-γ in Androstenediol-Mediated Salutary Effects on Cardiac Function Following Trauma-Hemorrhage

doi:10.1097/01.sla.0000217709.00863.82

Paper

A Role of PPAR-γ in Androstenediol-Mediated Salutary Effects on Cardiac Function Following Trauma-Hemorrhage

Published Jul 1, 2006 · Tomoharu Shimizu, L. Szalay, Y. Hsieh

Annals of Surgery

Q1 SJR score

22

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1

Influential Citations

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Abstract

Objective:To examine the mechanism by which androstenediol improves cardiac function following trauma-hemorrhage (T-H). Summary Background Data:Androstenediol administration improves cardiovascular function and attenuates proinflammatory cytokine production following T-H. Activation of the peroxisome proliferator-activated receptor-gamma (PPAR-γ) has been shown to be protective following ischemic conditions. We hypothesized that PPAR-γ activation plays a role in the androstenediol-mediated salutary effects on cardiac function following T-H. Methods:Male rats underwent laparotomy and hemorrhagic shock (40 mm Hg for 90 minutes), followed by resuscitation with 4 times the shed blood volume in the form of Ringer's lactate. Androstenediol (1 mg/kg body weight, i.v.) was administrated at the end of resuscitation. In a separate group of animals, a PPAR-γ antagonist (GW9662) was administered simultaneously with androstenediol and animals were killed at 5 hours thereafter. 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-γ DNA binding activity, attenuated IL-6 and iNOS gene expressions, and reduced plasma IL-6. Plasma 15-deoxy-Δ12, 14-prostaglandin J2 (PGJ2, an endogenous PPAR-γ agonist) levels were also increased in androstenediol-treated T-H rats, but these levels were lower than those observed in shams. Coadministration of PPAR-γ 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-γ activation, which down-regulates IL-6 and iNOS gene expression in the heart.

Non-RCT

Animal Study

Study Snapshot

Androstenediol improves cardiac function after trauma-hemorrhage by activating PPAR-, which down-regulates IL-6 and iNOS gene expression in the heart.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

A Role of PPAR-γ in Androstenediol-Mediated Salutary Effects on Cardiac Function Following Trauma-Hemorrhage

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References

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Sex steroid treatment restores cardiac function after trauma-hemorrhage, with decreased IL-6 synthesis in cardiomyocytes playing a key role in this process.

Citations

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