title: Ability of alpha-lipoic acid to reverse the diabetic cystopathy in a rat model.
abstract: OBJECTIVE
  The present study was conducted to investigate whether alpha-lipoic acid (alpha-LA) is able to reverse impaired bladder function induced by diabetes in a rat model and to explore the possible mechanism mediating the effect.
  
  
  METHODS
  Male Sprague-Dawley rats were divided randomly into 3 age-matched groups: control, diabetes mellitus (DM) treated with vehicle, and DM with alpha-LA treatment. The diabetic rats were induced by a single intraperitoneal (ip) injection of streptozotocin (60 mg/kg). Six weeks after the induction of DM, the two groups received another 6 weeks of treatment with vehicle or alpha-LA (100 mg/kg, i.p.). Body weight and blood glucose levels were measured weekly. The bladder function was evaluated by in vitro cystometry. The oxidative stress status was determined by biochemical methods, and the level of nerve growth factor was investigated by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  The streptozotocin-induced diabetic rats showed impaired bladder function characterized by increased bladder capacity, decreased bladder contractility (voiding efficiency), and an increase in residual urine. Treatment with alpha-LA significantly normalized the increased bladder capacity for inducing voiding, single-voided volume, and post-void residual volume. Alpha-LA treatment significantly reversed the increased level of malondialdehyde and reduced the activities of both superoxide dismutase and catalase. DM caused a decrease in the bladder nerve growth factor (NGF) level, and alpha-LA upregulated the level of NGF in the diabetic rat bladder.
  
  
  CONCLUSIONS
  These results indicate that alpha-LA has a beneficial effect on diabetes-induced cystopathy by ameliorating oxidative stress and normalizing the NGF level in the bladder.
authors.affiliation: Department of Urology, the First Affiliated Hospital, China Medical University, Shenyang 110001, China.
authors.forename: Yuan-jun
authors.initials: YJ
authors.lastname: Jiang
authors.forename: Da-xin
authors.initials: DX
authors.lastname: Gong
authors.forename: Hai-bo
authors.initials: HB
authors.lastname: Liu
authors.forename: Chun-ming
authors.initials: CM
authors.lastname: Yang
authors.forename: Zhi-xi
authors.initials: ZX
authors.lastname: Sun
authors.forename: Chui-ze
authors.initials: CZ
authors.lastname: Kong
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002374:Catalase / Q000378:metabolism; D048909:Diabetes Complications / Q000188:drug therapy* / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D020932:Nerve Growth Factor / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D008063:Thioctic Acid / Q000627:therapeutic use*; D001743:Urinary Bladder / Q000473:pathology; D001745:Urinary Bladder Diseases / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology
chemical_list: D000975:Antioxidants; D008315:Malondialdehyde; D008063:Thioctic Acid; D020932:Nerve Growth Factor; D002374:Catalase; D013482:Superoxide Dismutase