title: Acute 17β-estradiol pretreatment protects against abdominal aortic occlusion induced spinal cord ischemic-reperfusion injury.
abstract: Postoperative neurologic deficit due to spinal cord ischemia-reperfusion (I/R) injury is the most devastating complication following thoracoabdominal aortic aneurysm repairs. The protective potential for 17β-Estradiol has not been yet studied in such injury. In this study, ischemia induction for 18 min in male New Zealand White rabbits resulted in the highest percentage (80%) of biphasic paraplegic outcome assessed by Tarlov's score. Acute Estradiol pretreatment (1 mg/kg, i.p., 30 min before I/R induction) altered this outcome and significantly prevented the worsening pattern of neurologic deficits over 48 h of observation. Histopathologic and oxidative stress evaluations of lumbar spinal cords taken in delayed permanent paraplegic phase (48 h after ischemia induction), further confirmed protective efficacy of Estradiol in such context. In western blot analysis, the expression of cleaved caspase-3 and heat shock protein 70 declined in Estradiol pretreated group compared to ischemic control group. TUNEL assay also showed the efficacy of Estradiol to abate motor neuron apoptosis. Interestingly, Estradiol respectively increased and decreased the expression of Cyclooxygenase (COX)-1 and COX-2, to a significant extent. Estradiol, exerting its protection through affecting one or a combination of involved biochemical factors can constitute a potential candidate to protect against thoracoabdominal aortic aneurysm repairs induced spinal cord I/R injury.
authors.affiliation: Neuroscience Research Center, Pharmacology Department, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: Leila
authors.initials: L
authors.lastname: Khalaj
authors.forename: Habibollah
authors.initials: H
authors.lastname: Peirovi
authors.forename: Fariba
authors.initials: F
authors.lastname: Khodagholi
authors.forename: Azadeh
authors.initials: A
authors.lastname: Abdi
authors.forename: Leila
authors.initials: L
authors.lastname: Dargahi
authors.forename: Abolhassan
authors.initials: A
authors.lastname: Ahmadiani
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000601:surgery*; D017544:Aortic Aneurysm, Abdominal / Q000601:surgery; D053148:Caspase 3 / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004958:Estradiol / Q000627:therapeutic use*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D020287:In Situ Nick-End Labeling; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011817:Rabbits; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D020760:Spinal Cord Ischemia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D004958:Estradiol; D008315:Malondialdehyde; D002374:Catalase; D011451:Prostaglandin-Endoperoxide Synthases; D013482:Superoxide Dismutase; D053148:Caspase 3; D005978:Glutathione