Contribution of Testosterone in Attenuating Atherosclerotic Events and Adipose Tissue Inflammation in Male Rats
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- Category: Vol. 80, September 2012
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Contribution of Testosterone in Attenuating Atherosclerotic Events and Adipose Tissue Inflammation in Male Rats,MAGDA M. EL-HAMZAWY, HEBA M. SHAWKY, HANY EL-SEBAIE, HEBA S. SHOUKRY, LAILA A. RASHED, MAHA B. ZICKRI and HALA GABR
Abstract
The existence of a possible role of androgens has long been recognized in cardiovascular disorders in particular atherosclerosis. The aim of this study was to assess this role after castration and in response to testosterone replacement therapy (TRT) in an experimental rat model of atherosclerosis and to examine the impact of mechanisms involved. After 8 weeks of a hyperlipidemeic regimen, the castrated rats showed a highly significant elevation in the studied serum lipid profiles (total cholesterol (TC) and triglycerides (TG) and the inflammatory markers [high sensitivity C-reactive protein (CRP) and interleukin-6 (IL-6)] compared to sham-operated hyperlipidemic animals (p<0.01), whereas serum adiponectin was markedly reduced. At tissue level, the vascular and adipose tissue displayed a significant increase in IL-6 gene expressed levels and in the inflammatory cell infiltration (macrophages and foam cells) in contrast to sham operated rats, Also marked deterioration was depicted in the gene expressed levels of estrogen receptor alpha (ER-a) and adiponectin receptor (ADEPR1) rather than ADEPR2 (p<0.01). Supplying the castrated hyperlipidemic rats with TRT with or without aromataze inhibitor (Letrazole) resulted in a significant attenuation of the pathogenic events, which was reflected in the significant reduction of studied serum lipid profile and inflammatory markers and the marked increase in the adiponectin levels. Histological and biochem-ical analysis also revealed marked decrease of IL-6 gene expressed levels with significant decreased infiltration of inflammatory cells in adipose and vascular tissue (p<0.05). On the other hand, the ER-a and adiponectin receptor 1 showed upregulation in their gene expressed levels (p<0.01) although these results were observed to be less significant after the aromatase inhibition with letrazole. In conclusion the present study confirms a potential role of androgen in atheroprotection via an androgen receptor mediated action as well as through mechanisms initiated by its aromatization to estrogen.