Bradykinin preconditioning affects the number of degenerated neurons and the level of antioxidant enzymes in spinal cord ischemia in rabbits

• Published in: Acta histochemica Vol. 116; no. 1; pp. 252 - 257
• Main Authors: Mechírová, Eva, Danielisová, Viera, Domoráková, Iveta, Danková, Marianna, Stebnický, Milan, Mičková, Helena, Burda, Jozef
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.01.2014
• Subjects: Animals; Antioxidants - metabolism; Bradykinin - pharmacology; Bradykinin preconditioning; Catalase - metabolism; Fluoro Jade B; Ischemia - drug therapy; Ischemia - enzymology; Ischemia - pathology; Ischemic Preconditioning; Male; Nerve Degeneration - enzymology; Nerve Degeneration - prevention & control; Neurons - drug effects; Neurons - metabolism; Neuroprotective Agents - pharmacology; Rabbit; Rabbits; SOD; Spinal Cord - blood supply; Spinal Cord - drug effects; Spinal Cord - enzymology; Spinal cord ischemia; Superoxide Dismutase - metabolism; Br; Spinal cord ischemia; Mn-SOD; Bradykinin preconditioning; ROS; Rabbit; CNS; SOD; CuZn-SOD; Fluoro Jade B; FJB
• ISSN: 0065-1281; 1618-0372
• DOI: 10.1016/j.acthis.2013.07.010

Bradykinin preconditioning has been used for acquisition of tolerance after spinal cord ischemia. Rabbits were preconditioned intraperitoneally with bradykinin 48h prior to 20min of abdominal aorta ligation followed by 24 and 48h of reperfusion. The activities of SOD and catalase were measured and Fluoro Jade B (FJB)-positive degenerated neurons were evaluated. The outcomes of Tarlov scoring system used to assess neurological functions showed significant improvement in bradykinin groups compared to the ischemic group. The number of FJB-positive degenerated neurons was decreased in ventral horns of both bradykinin groups. Significantly decreased activities of total SOD and mitochondrial Mn-SOD were also detected in both bradykinin groups versus ischemic group while CuZn-SOD and catalase activities were significantly decreased only in the bradykinin group after 24h of reperfusion versus ischemic group. These findings suggest that one of the possibilities of the neuroprotective effect of delayed bradykinin preconditioning against spinal cord ischemic injury could be realized by mitochondrial protection and decreased synthesis of Mn-SOD as well as by promotion of neuronal survival.