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Sex hormones and neurovascular prote...

University of California, Irvine.

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Sex hormones and neurovascular protection: Modulation of inflammation and mitochondrial oxidative stress.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Sex hormones and neurovascular protection: Modulation of inflammation and mitochondrial oxidative stress./
Author:	Razmara, Ali.
Description:	267 p.
Notes:	Adviser: Sue P. Duckles.
Contained By:	Dissertation Abstracts International68-04B.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3260732

Sex hormones and neurovascular protection: Modulation of inflammation and mitochondrial oxidative stress.
Razmara, Ali.

Sex hormones and neurovascular protection: Modulation of inflammation and mitochondrial oxidative stress. - 267 p.

Adviser: Sue P. Duckles.

Thesis (Ph.D.)--University of California, Irvine, 2007.

Inflammation and mitochondrial oxidative stress are key paradigms in age-related disorders. Since there is a sex disparity in these diseases, it is important to elucidate sex hormone impact on cerebral vascular health in light of recent controversies surrounding hormone replacement therapy. We utilized in vivo models of animal hormone treatments and in vitro endothelial cells in culture to investigate physiologic effects of sex hormones on inflammation and mitochondrial oxidative stress.Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Sex hormones and neurovascular protection: Modulation of inflammation and mitochondrial oxidative stress.
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008 100709s2007 ||||||||||||||||| ||eng d
035 $a (UMI)AAI3260732
035 $a AAI3260732
040 $a UMI $c UMI
100 1 $a Razmara, Ali. $3 1023814
245 1 0 $a Sex hormones and neurovascular protection: Modulation of inflammation and mitochondrial oxidative stress.
300 $a 267 p.
500 $a Adviser: Sue P. Duckles.
500 $a Source: Dissertation Abstracts International, Volume: 68-04, Section: B, page: 2279.
502 $a Thesis (Ph.D.)--University of California, Irvine, 2007.
520 $a Inflammation and mitochondrial oxidative stress are key paradigms in age-related disorders. Since there is a sex disparity in these diseases, it is important to elucidate sex hormone impact on cerebral vascular health in light of recent controversies surrounding hormone replacement therapy. We utilized in vivo models of animal hormone treatments and in vitro endothelial cells in culture to investigate physiologic effects of sex hormones on inflammation and mitochondrial oxidative stress.
520 $a Chapter 2 describes the impact of sex hormones on cerebrovascular inflammation. Western analysis showed induction of inflammatory markers was increased in testosterone-treated rats. In contrast, estrogen significantly decreased endotoxin-induced COX-2 and NOS. Endotoxin increased COX-2 and iNOS immunoreactivity in endothelial and smooth muscle cells. In vitro incubation with endotoxin also induced COX-2 levels and PGE2 in isolated cerebral vessels, with the greatest induction in testosterone-treated rats. Chapter 3 explores the influence of sex hormones on brain mitochondrial oxidative stress. Estrogen decreased mitochondrial superoxide in differentiated PC-12 cells via the ER. After animal hormone treatments in vivo, we measured aconitase activity, a functional indicator of mitochondrial ROS. Gonadectomy caused a decrease in aconitase activity, and while androgens had no effect, estrogen increased aconitase activity in both female and male rats, indicating decreased mitochondrial ROS. Sex hormones did not affect levels of uncoupling proteins. However, MnSOD activity, but not protein, was higher in both female and male rats after estrogen treatment.
520 $a Chapter 4 investigates the impact of estrogen on mitochondrial ROS in cultured human brain microvascular endothelial cells. Using MitoSOX Red, 17beta-estradiol decreased mitochondrial superoxide production through ERa. Activity of aconitase was also increased by 17beta-estradiol, confirming less mitochondrial ROS. Tamoxifen and raloxifene also showed differential effects on mitochondrial superoxide production. Moreover, 17beta-estradiol increased cytochrome c through ERa and the PGC-1 transcriptional co-activators via the ER.
520 $a In conclusion, sex hormones impact neurovascular protection by modulating inflammation and mitochondrial oxidative stress. The ability of estrogen to suppress cerebrovascular inflammation and mitochondrial ROS may influence neurological disease incidence and progression. These profound effects of estrogen may contribute to sex differences in lifespan and may provide insight into the development of new therapies.
590 $a School code: 0030.
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
710 2 $a University of California, Irvine. $3 705821
773 0 $t Dissertation Abstracts International $g 68-04B.
790 $a 0030
790 1 0 $a Duckles, Sue P., $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3260732