Sulforaphane Improves Ischemia-Induced Detrusor Overactivity by Downregulating the Enhancement of Associated Endoplasmic Reticulum Stress, Autophagy, and Apoptosis in Rat Bladder

摘要: Atherosclerosis-associated pelvic ischemia has been reported to be a risk factor for bladder dysfunction and subsequent lower urinary tract symptoms (LUTS) in the elderly population. However, molecular mechanisms of this association remain unclear. We hypothesized that stress-induced cellular responses might play role pathogenesis ischemia-induced dysfunction. In present study, animal model was induced by bilateral partial arterial occlusion (BPAO) rats. found BPAO significantly presence detrusor overactivity (DO) upregulated expression several reactions, including biomarkers endoplasmic reticulum stress (78 kDa glucose-regulated protein, GRP78 C/EBP-homologous CHOP), autophagy (Beclin-1, p62 LC3 II) apoptosis (caspase 3). also disturbed Kelch-like ECH-associated protein 1–nuclear erythroid-2-related 2 (Keap1–Nrf2) pathways. These collectively alter muscarinic purinergic signaling contribute DO ischemic bladder. Therapeutically, treatment with neither nor receptor antagonist restored function. Interestingly, sulforaphane effectively attenuated ischemia-enhanced stress, bladder, subsequently ameliorated emerge as novel strategy protect against oxidative damage.