Effects of 17 beta-estradial on cardiac apoptosis in ovariectomized rats

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Title:	Effects of 17 beta-estradial on cardiac apoptosis in ovariectomized rats
Authors:	黃志揚;HUANG, CHIH-YANG;李信達;Lee, Shin-Da
Contributors:	生物科技學系
Date:	2010-07
Issue Date:	2012-11-23 09:13:25 (UTC+0)
Abstract:	OBJECTIVES: Cardiac apoptosis was found in ovariectomized rats without ischemia. Limited information regarding the protective effects of 17beta-estradiol (E2) on cardiac Fas-dependent and mitochondria-dependent apoptotic pathways after post-menopause or bilateral oophorectomy in women was available. METHODS: Forty-eight female Wistar rats at 6-7 months of age were divided into sham-operated group (Sham, n = 16) and bilateral ovariectomized group (n = 32). After 4 weeks of operation, rats in ovariectomized group were injected intraperitoneally with either saline (OVX, n = 16) or 10 microg/kg/day 17beta-estradiol (E2) for 10 weeks (OVX-E2, n = 16). The excised hearts were measured by Hematoxylin-eosin staining, DAPI staining, positive TUNEL assays, and Western Blotting. RESULTS: 17beta-estradiol (E2) decreased OVX-induced cardiac widely dispersed TUNEL-positive apoptotic cells. 17beta-estradiol (E2) decreased OVX-induced TNF-alpha, Fas ligand (Fas L), Fas death receptors (Fas), Fas-associated death domain (FADD), activated caspase 8, and activated caspase 3 (Fas pathways). 17beta-estradiol (E2) decreased OVX-induced proapoptotic t-Bid, Bax, Bax-to-Bcl2 ratio, Bax-to-BclXL ratio, activated caspase 9, and activated caspase 3 as well as increased anti-apoptotic Bcl2 and Bcl-XL relative to OVX (mitochondria pathway). CONCLUSIONS: Our findings suggest that chronic 17beta-estradiol (E2) treatment can prevent ovariectomy-induced cardiac Fas-dependent and mitochondria-dependent apoptotic pathways in rat models. The findings may provide one of possible mechenisms of 17beta-estradiol (E2) for potentially preventing cardiac apoptosis after bilateral ovariectomy or menopause.
Relation:	CELL BIOCHEMISTRY AND FUNCTION;28(6):521-8.
Appears in Collections:	[Department of Biotechnology] Journal Article

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