The attenuation of neurological injury from the use of simvastatin after spinal cord ischemia-reperfusion injury in rats

Autor: Jung-Hee Ryu, Jin-woo Park, Jin-Young Hwang, Seong-Joo Park, Jin-Hee Kim, Hye-Min Sohn, Sung Hee Han
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Zdroj: BMC Anesthesiology, Vol 18, Iss 1, Pp 1-7 (2018)
Druh dokumentu: article
ISSN: 1471-2253
DOI: 10.1186/s12871-018-0496-6
Popis: Abstract Background Spinal cord ischemic injury remains a serious complication of open surgical and endovascular aortic procedures. Simvastatin has been reported to be associated with neuroprotective effect after spinal cord ischemia-reperfusion (IR) injury. The aim of this study was to determine the therapeutic efficacy of starting simvastatin after spinal cord IR injury in a rat model. Methods In adult Sprague-Dawley rats, spinal cord ischemia was induced using a balloon-tipped catheter placed in the descending thoracic aorta. The animals were then randomly divided into 4 groups: group A (control); group B (0.5 mg/kg simvastatin); group C (1 mg/kg simvastatin); and group D (10 mg/kg simvastatin). Simvastatin was administered orally upon reperfusion for 5 days. Neurological function of the hind limbs was evaluated for 7 days after reperfusion and recorded using a motor deficit score (MDS) (0: normal, 5: complete paraplegia). The number of normal motor neurons within the anterior horns of the spinal cord was counted after final MDS evaluation. Then, the spinal cord was harvested for histopathological examination. Results Group D showed a significantly lower MDS than the other groups at post-reperfusion day 1 and this trend was sustained throughout the study period. Additionally, a greater number of normal motor neurons was observed in group D than in other groups (group D 21.2 [3.2] vs. group A: 15.8 [4.2]; group B 15.4 [3.4]; and group C 15.5 [3.7]; P = 0.002). Conclusions The results of the current study suggest that 10 mg/kg can significantly improve neurologic outcome by attenuating neurologic injury and restoring normal motor neurons after spinal cord IR injury.
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