In:
Cell Biochemistry and Function, Wiley, Vol. 28, No. 6 ( 2010-08), p. 521-528
Kurzfassung:
Cardiac apoptosis was found in ovariectomized rats without ischemia. Limited information regarding the protective effects of 17β‐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 µg/kg/day 17β‐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 17β‐estradiol (E2) decreased OVX‐induced cardiac widely dispersed TUNEL‐positive apoptotic cells. 17β‐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). 17β‐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 17β‐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 17β‐estradiol (E2) for potentially preventing cardiac apoptosis after bilateral ovariectomy or menopause. Copyright © 2010 John Wiley & Sons, Ltd.
Materialart:
Online-Ressource
ISSN:
0263-6484
,
1099-0844
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2010
ZDB Id:
1496553-7
SSG:
12
