https://scholars.lib.ntu.edu.tw/handle/123456789/193607
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor | 泌尿科 | en |
dc.contributor.author | YU, HONG-JENG | en |
dc.contributor.author | CHIEN, CHIANG-TING | en |
dc.contributor.author | LAI, YU-JEN | en |
dc.contributor.author | LAI, MING-KUEN | en |
dc.contributor.author | CHEN, CHAU-FONG | en |
dc.contributor.author | ROBERT M. LEVIN | en |
dc.contributor.author | HSU, SU-MING | en |
dc.contributor.author | 余宏政 | zh-tw |
dc.contributor.author | 鄭劍廷 | zh-tw |
dc.contributor.author | 賴怡君 | zh-tw |
dc.contributor.author | 賴明坤 | zh-tw |
dc.contributor.author | 陳朝峰 | zh-tw |
dc.contributor.author | 許世明 | zh-tw |
dc.creator | 余宏政;鄭劍廷;賴怡君;賴明坤;陳朝峰;許世明 | zh-tw |
dc.creator | YU, HONG-JENG;CHIEN, CHIANG-TING;LAI, YU-JEN;LAI, MING-KUEN;CHEN, CHAU-FONG;ROBERT M. LEVIN;HSU, SU-MING | en |
dc.date | 2004 | en |
dc.date.accessioned | 2009-01-16T03:14:17Z | - |
dc.date.accessioned | 2018-07-11T17:07:11Z | - |
dc.date.available | 2009-01-16T03:14:17Z | - |
dc.date.available | 2018-07-11T17:07:11Z | - |
dc.date.issued | 2004 | - |
dc.identifier.uri | http://ntur.lib.ntu.edu.tw//handle/246246/97156 | - |
dc.description.abstract | We explored whether hypoxic preconditioning minimizes oxidative injury induced by overdistension/emptying in the rat bladder. For hypoxic preconditioning, female Wistar rats were placed in a hypobaric chamber ( 380 Torr) 15 h/day for 28 days. Overdistension was in-duced by infusion of two times the threshold volume of saline into the bladder and was main- tained for 1 or 2 h, followed by drainage/emptying. During overdistension (ischemia) and emptying (reperfusion) periods, a bursting increase of reactive oxygen species ( ROS) from the bladder was originated from the large numbers of infiltrating leukocytes and scattered resident cells, including urothelial, submucosal, and smooth muscle cells. ROS impaired the voiding function by a reduction of bladder afferent and efferent nerve activity and acetylcholine- or ATP-induced detrusor contraction. ROS enhanced pro-apoptotic mechanisms, including in-creases in the Bax/Bcl-2 ratio, CPP32 expression, and PARP fragments with subsequent apop- totic cell formation in the insulted bladders. Hypoxia preconditioning upregulated Bcl-2 ex-pression in the bladder and significantly reduced the levels of ROS and apoptosis detected in the overdistension/emptying bladders and preserved partial voiding function. In conclusion, Bcl-2 upregulation by hypoxia preconditioning contributes protection against overdisten-sion/emptying-induced oxidative stress and injury in the bladder. | en |
dc.language | en-us | en |
dc.language.iso | en_US | - |
dc.relation | THE JOURNAL OF PHYSIOLOGY (LONDON) v.554 n.3 pp.815-828 | en |
dc.relation.ispartof | THE JOURNAL OF PHYSIOLOGY (LONDON) | - |
dc.subject | Hypoxia preconditioning | en |
dc.subject | Bladder overdistension | en |
dc.subject | Oxidative s | en |
dc.title | Hypoxia Preconditioning Attenuates Bladder Overdistension-Induced Oxidative Injury by Upregulation of Bcl-2 in the Rat. | en |
dc.title | 低氧前置處理可經由 增加bcl-2的調控而降低大白鼠膀胱過度膨脹所導致的過氧化傷害 | zh-tw |
dc.relation.pages | 815-828 | - |
dc.relation.journalvolume | v.554 | - |
dc.relation.journalissue | n.3 | - |
item.languageiso639-1 | en_US | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
顯示於: | 醫學系 |
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