کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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4326842 | 1614097 | 2010 | 10 صفحه PDF | دانلود رایگان |

The current study was performed to investigate the effect of aminoguanidine (AG) on spinal cord injury (SCI) in rat. AG (75, 150 and 300 mg/kg, i.p. respectively ) was administered to rats immediately following SCI. It was found that AG (150 mg/kg) significantly reduced spinal cord water content and improved motor function, however, AG at the doses of 75 and 300 mg/kg had no effect. Compared to SCI group without treatment, AG at the dosage of 150 mg/kg induced a reduction in the permeability of blood–spinal cord barrier (BSCB) after injury 48 h (from 59.8 ± 5.5 µl/g to 39.8 ± 3.8 µl/g), a 38% decrease of Malondialdehyde (MDA) values and a 1-fold increase of the Glutathione (GSH) levels at 12 h after SCI. And the expression of inducible nitric oxide synthase (iNOS) protein reached a peak at 24 h after injury, which was significantly attenuated by treatment with AG (150 mg/kg). In addition, the expression of AQP4 protein was down-regulated by the treatment of AG (150 mg/kg) at 24 h after SCI, and the changes still lasted at 48 h after injury. Our results indicated that AG could induce spinal cord edema clearance and improve motor function, which could be correlated with antioxidative property, the down-regulation of iNOS and AQP4 protein expression after SCI.
Journal: Brain Research - Volume 1342, 25 June 2010, Pages 1–10