|Title:||Bcl-2 基因過度表現對於物質P誘發膀胱功能亢進的影響||Authors:||余宏政||Issue Date:||2004||Publisher:||臺北市：國立臺灣大學醫學院泌尿科||Abstract:||
物質P 可以誘發過動膀胱是因其透過ICAM 與活性氧之作用。這些作用可以受抗氧化
物質補充而改善。我們以誘發 Bcl-2 portein 的結果發現可以改善之。同時也可以減低
發炎、過度收縮與細胞凋亡現象。此二篇相關文章已發表於Am J Physiol 與J Physiol
We explored whether substance P (SP) via neurokinin (NK) receptor facilitates bladder
afferent signaling and reactive oxygen species (ROS) formation in bladder connected with
neurogenic inflammation. We evaluated ROS activity and cystometrograms as well as
pelvic nervous activity in anesthetized rat bladder with SP stimulation. Our results showed
endogenous SP via NK1, not NK2 receptor in mediating a micturition reflex. Increased SP
by electrical stimulation of pelvic nerve or exogenous SP from intra-arterial or spinal route
can facilitate myogenic and neurogenic bladder contractions. Furthermore, exaggerated SP
release caused an increase in ROS amounts in the bladder and whole blood with the
mechanism of increased mast cell degranulation, intercellular adhesion molecule (ICAM)
expression, and leukocytes adhesion, a primary source of ROS in the inflamed bladder.
Treatment with NK1 receptor antagonist or ROS scavengers reduced the bladder ICAM
expression and ROS amounts, and ameliorated the hyperactive bladder response. Our study
indicates that the mechanism by which SP participates in the neurogenic bladder may be
complicated by its proinflammatory activity and its ability to stimulate ROS generation.
|Appears in Collections:||醫學系|
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