東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Amelioration of oxidative stress in ...

The University of Texas at Austin., Pharmacy.

Linked to FindBook

Google Book

Amazon

博客來

Amelioration of oxidative stress in human endothelial cells by caffeic acid phenethyl ester (CAPE) and fluorinated derivatives (FCAPES) and pharmacokinetic characterization of CAPE and FCAPE in rats.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Amelioration of oxidative stress in human endothelial cells by caffeic acid phenethyl ester (CAPE) and fluorinated derivatives (FCAPES) and pharmacokinetic characterization of CAPE and FCAPE in rats./
Author:	Wang, Xinyu.
Description:	241 p.
Notes:	Adviser: Salomon Stavchansky.
Contained By:	Dissertation Abstracts International68-12B.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3290913
ISBN:	9780549350248

Amelioration of oxidative stress in human endothelial cells by caffeic acid phenethyl ester (CAPE) and fluorinated derivatives (FCAPES) and pharmacokinetic characterization of CAPE and FCAPE in rats.
Wang, Xinyu.

Amelioration of oxidative stress in human endothelial cells by caffeic acid phenethyl ester (CAPE) and fluorinated derivatives (FCAPES) and pharmacokinetic characterization of CAPE and FCAPE in rats. - 241 p.

Adviser: Salomon Stavchansky.

Thesis (Ph.D.)--The University of Texas at Austin, 2007.

Tissue ischemia is a major cause of morbidity contributing to disease processes such as cardiovascular diseases, stroke, cancer, and traumatic injury and may lead to death. Failure to quickly reestablish flow to ischemic tissue results in tissue death. However, even timely return to normal flow has a downside in that the reintroduction of oxygen to ischemic tissue results in ischemia/reperfusion (I/R) injury that produces an oxidant stress. This pathological process requires new therapeutic strategies and agents to reduce the personal, social and economic loss. One of the most generally accepted mechanisms for the pathology of I/R injury is the production of the reactive oxygen species (ROS), suggesting antioxidants may ameliorate I/R injury.

ISBN: 9780549350248Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Amelioration of oxidative stress in human endothelial cells by caffeic acid phenethyl ester (CAPE) and fluorinated derivatives (FCAPES) and pharmacokinetic characterization of CAPE and FCAPE in rats.
LDR:03776nam 2200301 a 45 001 855183
005 20100708
008 100708s2007 ||||||||||||||||| ||eng d
020 $a 9780549350248
035 $a (UMI)AAI3290913
035 $a AAI3290913
040 $a UMI $c UMI
100 1 $a Wang, Xinyu. $3 1021717
245 1 0 $a Amelioration of oxidative stress in human endothelial cells by caffeic acid phenethyl ester (CAPE) and fluorinated derivatives (FCAPES) and pharmacokinetic characterization of CAPE and FCAPE in rats.
300 $a 241 p.
500 $a Adviser: Salomon Stavchansky.
500 $a Source: Dissertation Abstracts International, Volume: 68-12, Section: B, page: 7955.
502 $a Thesis (Ph.D.)--The University of Texas at Austin, 2007.
520 $a Tissue ischemia is a major cause of morbidity contributing to disease processes such as cardiovascular diseases, stroke, cancer, and traumatic injury and may lead to death. Failure to quickly reestablish flow to ischemic tissue results in tissue death. However, even timely return to normal flow has a downside in that the reintroduction of oxygen to ischemic tissue results in ischemia/reperfusion (I/R) injury that produces an oxidant stress. This pathological process requires new therapeutic strategies and agents to reduce the personal, social and economic loss. One of the most generally accepted mechanisms for the pathology of I/R injury is the production of the reactive oxygen species (ROS), suggesting antioxidants may ameliorate I/R injury.
520 $a Caffeic acid phenethyl ester (CAPE), a plant derived polyphenolic compound, has been shown to protect organs from I/R induced damage in vivo, and this effect has been attributed to its antioxidant activity. To better understand the mechanism of CAPE protection, a model using menadione-induced oxidative stress in human endothelial cells to simulate I/R injury in vitro was developed. Gene expression analysis was performed with microarrays undergoing cytoprotection with CAPE. The dose-dependent cytoprotection of CAPE has been related to its induction of heme oxygenase-1 (HO-1).
520 $a With the aim of improving the beneficial effect of CAPE and understanding structure activity relationship, six new catechol ring-fluorinated CAPE derivatives were synthesized and evaluated in the menadione-endothelial cell model. The data suggest good cytoprotective effects of CAPE and some analogues and indicate important structural features for cytoprotection. Further investigation of the mechanism of cytoprotection showed that cytoprotection profiles of CAPE and derivatives correlate better to their ability to induce HO-1 in human endothelial cells than free radical scavenging activity.
520 $a One CAPE derivative (FCAPE) with cytoprotective effects similar to CAPE in vitro exhibited better stability in rat plasma. A validated ultra-performance liquid chromatography/tandem mass spectrometric method was developed that allowed for quantification of CAPE and FCAPE in plasma samples. Pharmacokinetic studies in male Sprague Dawley rats following intravenous bolus administration of 5, 10, and 20 mg/kg CAPE and 20 mg/kg FCAPE were performed. The results indicate that dose proportionality for CAPE does not exist in the dose range studied. Although the elimination half life was found not to be significant different between CAPE and FCAPE, significant difference was observed between the total body clearance of FCAPE and CAPE which may due to the difference in volume of distribution.
590 $a School code: 0227.
650 4 $a Health Sciences, Pharmacology. $3 1017717
690 $a 0419
710 2 $a The University of Texas at Austin. $b Pharmacy. $3 1021716
773 0 $t Dissertation Abstracts International $g 68-12B.
790 $a 0227
790 1 0 $a Stavchansky, Salomon, $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3290913