Neuroprotective effect of mesna (2-mercaptoethane sulfonate) against spinal cord ischemia/reperfusion injury in rabbits

被引:23
|
作者
Dolgun, Habibullah [1 ]
Sekerci, Zeki [1 ]
Turkoglu, Erhan [1 ]
Kertmen, Hayri [1 ]
Yilmaz, Erdal R. [1 ]
Anlar, Murat [2 ]
Erguder, Imge B. [3 ]
Tuna, Hakan [4 ]
机构
[1] Diskapi Yildirim Beyazit Educ & Res Hosp, Neurosurg Clin 1, Ankara, Turkey
[2] Diskapi Yildirim Beyazit Educ & Res Hosp, Pathol Clin 2, Ankara, Turkey
[3] Ankara Univ, Fac Med, Dept Biochem, TR-06100 Ankara, Turkey
[4] Ankara Univ, Fac Med, Dept Neurosurg, TR-06100 Ankara, Turkey
关键词
Apoptosis; Caspase; Ischemia/reperfusion injury; Mesna; 2-Mercaptoethane sulfonate; DELAYED NEURONAL DEATH; CELL-DEATH; CASPASE-3; INHIBITOR; TEMPORAL PROFILE; MOTOR-NEURONS; ISCHEMIA; RATS; MECHANISMS; APOPTOSIS; INDUCTION;
D O I
10.1016/j.jocn.2009.07.108
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Although the precise mechanism by which ischemia/reperfusion injury occurs in the spinal cord remains unclear, it is evident that free oxygen radicals and apoptosis play major roles in the destruction of membrane lipids, damage to DNA and cell death. The apoptotic process involves activation of the caspase-3 cascade. Although it is widely used as a protective agent against cell injury, it is unknown whether mesna (2-mercaptoethane sulfonate) ameliorates neuronal ischemic injury. The aim of this study was to determine the effect of mesna on caspase-3 activity in a rabbit model. Adult rabbits underwent spinal cord ischemic injury via occlusion of the abdominal aorta for 20 min. Twenty-four hours after ischemia, spinal cord samples were obtained and tissue caspase-3 activity was measured. Rabbits that had been given a single dose of 150 mg/kg mesna had decreased caspase-3 activity in the spinal cord following ischemia/reperfusion injury, indicating a protective effect. However, caspase-3 activity was lower in rabbits given methylprednisolone than in those given mesna, indicating that methylprednisolone has the stronger protective effect of the two agents. Published by Elsevier Ltd.
引用
收藏
页码:486 / 489
页数:4
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