OBJECTIVE: To study the effects of aminoguanidine (AG), the inhibitor of inducible nitric oxide synthase (NOS), on the recovery of rat hindlimb motor function after spinal cord injury and explore the possible mechanism. METHODS: Thirty rat models of spinal cord compression injury were established according to Nystrom's method. AG therapy was administered for 4 times at 1 h before and 8, 24, 36 h after the injury, and 24 h after the completion of the therapy, spectrophotography was performed to measure the content of NO and activity of NOS in the injured spinal cord, followed by flow cytometry for determining the apoptotic rate 48 h later. The evaluation of the hindlimb motor function recovery was conducted by electrophysiological method and by measuring the behavior scores. RESULTS: AG significantly decreased the NO content (from 2.2714+/-0.4239 micromol/g.pro to 0.8466+/-0.0477 micromol/g.pro, P <0.05) and NOS activity (from 0.3408+/-0.0228 U/mg pro to 0.2702+/-0.0148 U/mg pro, P <0.05) in the injured spinal cord. The apoptotic rats were also reduced (from 7.88% +/-0.79% to 3.10% +/-0.66%, P <0.05). Four weeks after the therapy, the behavior score of the rats improved from 7.1+/-4.5 to 17.3+/-4.7 (P <0.01), and the latency and amplitude of the motor evoked potentials improved from 0 ms to 8.89+/-0.91 ms and from 0 mv to 1.99+/-0.48 mv respectively, showing significant therapeutic effect of AG (P <0.05). CONCLUSION: AG can improve motor functions of injured spinal cord in rats, possibly resulting from decreased apoptotic cells of the neurons in the spinal cord in the early stages of the injury.
OBJECTIVE: To study the effects of aminoguanidine (AG), the inhibitor of inducible nitric oxide synthase (NOS), on the recovery of rat hindlimb motor function after spinal cord injury and explore the possible mechanism. METHODS: Thirty rat models of spinal cord compression injury were established according to Nystrom's method. AG therapy was administered for 4 times at 1 h before and 8, 24, 36 h after the injury, and 24 h after the completion of the therapy, spectrophotography was performed to measure the content of NO and activity of NOS in the injured spinal cord, followed by flow cytometry for determining the apoptotic rate 48 h later. The evaluation of the hindlimb motor function recovery was conducted by electrophysiological method and by measuring the behavior scores. RESULTS: AG significantly decreased the NO content (from 2.2714+/-0.4239 micromol/g.pro to 0.8466+/-0.0477 micromol/g.pro, P <0.05) and NOS activity (from 0.3408+/-0.0228 U/mg pro to 0.2702+/-0.0148 U/mg pro, P <0.05) in the injured spinal cord. The apoptotic rats were also reduced (from 7.88% +/-0.79% to 3.10% +/-0.66%, P <0.05). Four weeks after the therapy, the behavior score of the rats improved from 7.1+/-4.5 to 17.3+/-4.7 (P <0.01), and the latency and amplitude of the motor evoked potentials improved from 0 ms to 8.89+/-0.91 ms and from 0 mv to 1.99+/-0.48 mv respectively, showing significant therapeutic effect of AG (P <0.05). CONCLUSION: AG can improve motor functions of injured spinal cord in rats, possibly resulting from decreased apoptotic cells of the neurons in the spinal cord in the early stages of the injury.