Coenzyme Q10 diminishes ischemia–reperfusion induced apoptosis and nerve injury in rabbit urinary bladder

Abstract

Ischemia/reperfusion (I/R) can significantly change the nerve function of the bladder, thus resulting in detrusor weakness and overactivity. CoQ10 is a lipid-soluble cofactor found naturally in the mitochondria and has been reported to have neuroprotective and antiapoptosis effects. The aim of this study is to determine if CoQ10 can protect bladders subjected to I/R injury. Four groups of male New Zealand White rabbits (N = 4) were treated with CoQ10 (3 mg/kg body weight/day) (groups 1 and 2) or vehicle (groups 3 and 4). In groups 2 and 4 (I/R groups), bilateral vesicular ischemia was induced for 2 hr and the rabbits allowed to recover for 2 weeks. Groups 1 and 3 were controls and given sham surgery. The cholinergic nerve marker, vesicular acetylcholine transporter (VAChT), was examined by western blotting. Nerve density and cell apoptosis were calculated by immunohistochemistry. I/R significantly decrease bladder innervation; CoQ10 has significant neuroprotective effects, which are evidenced by increased VAChT expression and neurofilament immunostaining. Detrusor cells apoptosis increase significantly by I/R. CoQ10 control and I/R groups both show significantly lower apoptosis than vehicle groups. The current study clearly demonstrated that these CoQ10 supplement provides significant bladder protection against I/R injury. This protective effect is in part by protecting damage to cholinergic innervation.