Studies have shown that endogenous @entity172 minimized cellular injury at the organ level; however, very little research was done to determine the effects of endogenous @entity3800 such as @entity251 (T), @entity586 , ( @entity587 ), and @entity2671 (AED) on the cardiovascular system at the cellular level Studies targeted at establishing such effects will broaden our understanding of the roles played by these male @entity134 hormones on the cardiovascular system. Our objective therefore was to (1) Use a @entity35 model and sustained delivery of physiological levels of these hormones to (1) evaluate pathophysiological effects on the cardiovascular system; and (2) localized cytokines such as IL-1, @entity568 and @entity1505 on these tissues. Four groups of @entity35 were included in the study. Group 1 animals served as control, groups II, III, and IV were treated with TCPL drug delivery devices containing 40 mg each of T, @entity587 , and AED, respectfully. Animals were sacrificed after 90 days of exposure. The ventricles and apex were immunostained for IL-1, @entity568 , @entity1505 and were also stained with @entity1710 and Eosin for histopathological evaluation. Results showed that TCPL drug delivery systems released 5 ng/ml/day of T, and 2 ng/ml/day of @entity587 and AED. @entity568 was expressed in the control heart ventricle and T, @entity587 , and AED reduced expression of the cytokine significantly after 90 days. Very small number of cells from the apex responded to @entity568 than cells within the ventricles. The results revealed that (i) the exposure of sustained levels of androgenic hormones exhibited myocardial @entity1184 compared to the control animals, (ii) the control animals had a two-fold increase in the ventricles @entity568 production over T treated animals and approximately five-fold increase over @entity587 and AED treated animals, and (iii) other inflammatory cytokines @entity1505 were not differentially expressed in the ventricles of experimental animals when compared with the control; and (iv) In the apex tissue, animals treated with AED exhibited cells with increased response to @entity568 and a decrease cells responding to @entity1505 and IL-1. @entity568 production in the ventricles decreased in animals exposed to sustained androgenic @entity230 and this decrease could possibly lead to increased blood flow, resulting in better oxygenation of the myocardium and improved cardiac function.

Localization of cytokines in heart ventricular and apex tissues exposed to sustained delivery of AED, T, and @entity587 using a XXXX model.

@entity172 :: ('MESH:D004967', 'Chemical') :: ['estrogen'] @entity230 :: ('MESH:D013256', 'Chemical') :: ['steroids'] @entity251 :: ('MESH:D013739', 'Chemical') :: ['Testosterone'] @entity586 :: ('MESH:D013196', 'Chemical') :: ['Dihydrotestosterone'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophic condition'] @entity568 :: ('24498(Tax:10116)', 'Gene') :: ['IL-6'] @entity1505 :: ('24835(Tax:10116)', 'Gene') :: ['TNF', 'IL-1 and TNF'] @entity2671 :: ('MESH:D000735', 'Chemical') :: ['Androstenedione'] @entity134 :: ('CHEBI:35341', 'Chemical') :: ['steroid'] @entity1710 :: ('MESH:D006416', 'Chemical') :: ['Hemotoxylin'] @entity35 :: ('10116', 'Species') :: ['Sprague Dawley rats', 'Rat'] @entity587 :: ('CHEBI:16330', 'Chemical') :: ['DHT'] @entity3800 :: ('MESH:D000728', 'Chemical') :: ['androgens']
@entity35 :: (10116,Species) :: ['rat']
