on October 19, 2006
Published online before print October 19, 2006, doi: 10.1161/01.STR.0000249008.18669.5a
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Submitted on June 12, 2006
From Graduate Institute of Medicine (H.-C.S., C.-L.L.), and Departments of Neurosurgery (C.-L.L.) and Physiology (T.-Y.L., W.-S.L., C.H.), College of Medicine, Kaohsiung Medical University, Taiwan; Graduate Institute of Medical Sciences (W.-S.L.), Medical College, Taipei Medical University, Taiwan. * To whom correspondence should be addressed. E-mail: chinhsu{at}cc.kmu.edu.tw.
Background and Purpose--Previously, we showed that 17 Methods--The 2-hemorrhage SAH model was induced by 2 autologous injections of blood into the cisterna magna of adult male rats. The rats were then subcutaneously implanted of a Silastic tube containing corn oil with or without 17 Results--E2 prevented the SAH-induced vasospasm and increases of the levels of iNOS protein and mRNA in basilar artery through an ER-dependent mechanism. Treatment of the SAH rat with E2 did not affect the nuclear translocation of p65 subunit of nuclear factor Conclusions--E2 inhibits the SAH-induced increase of iNOS by increasing the association of p65/ER, which in turn inhibits the binding of p65 to iNOS DNA. Our data suggest the potential applications of E2 in the treatment of SAH patient.
Revised on July 28, 2006
Accepted on August 14, 2006
17
Huei-Chuan Shih MS; 
-Estradiol Inhibits Subarachnoid Hemorrhage-Induced Inducible Nitric Oxide Synthase Gene Expression by Interfering With the Nuclear Factor 
B Transactivation
-estradiol (E2) treatment prevented the subarachnoid hemorrhage (SAH)-induced cerebral vasospasm in male rats. The aim of this study was designed to further delineate the molecular mechanisms underlying E2-induced inhibition of inducible nitric oxide synthase (iNOS) upregulation and relief of vasospasm caused by SAH.-estradiol benzoate and received daily intraperitoneal injections of various doses of ICI 182,780, a nonselective estrogen receptor (ER) antagonist, for 7 days after the first hemorrhage. Basilar arteries were then removed for protein extraction, RNA isolation, and gel mobility assay. The protein levels of iNOS, p65, and ER were examined by Western blot analysis, and that iNOS mRNA expression was evaluated by reverse-transcription polymerase chain reaction.
B, but caused an increase of the association of p65/ER, and reversed the SAH-induced increase of the p65 binding on iNOS promoter.
Key words: estradiol • iNOS • nuclear factor
B •
subarachnoid hemorrhage •
stroke
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