Pii: S1010-7940(99)00246-8

نویسندگان

  • Atilla Ilhan
  • Ugur Koltuksuz
  • Suleyman Ozen
  • Efkan Uz
  • Harun Ciralik
  • Omer Akyol
چکیده

Objective: Oxygen-derived free radicals have been implicated in the pathogenesis of spinal cord neuronal injury after both trauma and ischemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. This experimental study was designed to determine the effect of CAPE on ischemia-reperfusion of spinal cord in rabbits. Methods: Forty-one New Zealand white rabbits were used in the study. The animals undergone aortic occlusion were divided into three groups each consisting of 11 rabbits: methylprednisolone (MP), CAPE, and control. CAPE 10 mmol/kg, methyl prednisolone (MP) 30 mg/kg or similar dose saline were injected intraperitoneally before surgical intervention. Animals were subjected to 21 min of cross-clamp time. At the end of occlusion time, the clamps were removed and restoration of the blood ̄ow was veri®ed visually. Animals in sham group (n ˆ 8) underwent a surgical procedure similar to the other groups but the aorta was not occluded. Neurological status was scored by assessment of hindlimb motor function de®cit. Results: The scores in CAPE group was different from control groups at 48 h (3:91 ^ 0:5 vs. 2:91 ^ 0:7; P ˆ 0:0013). Spinal cord specimens were obtained to determine the tissue levels of malondialdehyde, superoxide dismutase, catalase, and histological changes. Malondialdehyde levels in control group were increased signi®cantly when compared to sham group (124:22 ^ 24:36 and 41:92 ^ 10:08 nmol/g wet tissue, P ˆ 0:0003). MDA levels in the CAPE group were lower than MP group and differences between the two groups were statistically signi®cant (56:77 ^ 15:265 and 107:74 ^ 19:31 nmol/g wet tissue, P ˆ 0:0001). We did not observe additional tissue injury in CAPE group when compared to control group. SOD and CAT activities were not concordant in all the groups. Conclusions: These results suggest that CAPE may be an available agent to protect the spinal cord from ischemia-reperfusion injury. q 1999 Elsevier Science B.V. All rights reserved.

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تاریخ انتشار 1999