https://scholars.lib.ntu.edu.tw/handle/123456789/193607
標題: | Hypoxia Preconditioning Attenuates Bladder Overdistension-Induced Oxidative Injury by Upregulation of Bcl-2 in the Rat. 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 |
作者: | YU, HONG-JENG CHIEN, CHIANG-TING LAI, YU-JEN LAI, MING-KUEN CHEN, CHAU-FONG ROBERT M. LEVIN HSU, SU-MING 余宏政 鄭劍廷 賴怡君 賴明坤 陳朝峰 許世明 |
關鍵字: | Hypoxia preconditioning;Bladder overdistension;Oxidative s | 公開日期: | 2004 | 卷: | v.554 | 期: | n.3 | 起(迄)頁: | 815-828 | 來源出版物: | THE JOURNAL OF PHYSIOLOGY (LONDON) | 摘要: | 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. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/97156 |
顯示於: | 醫學系 |
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