Bcl-2 基因過度表現對於物質P誘發膀胱功能亢進的影響

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.