Wu W, Li L
Microsurgical Research Center, Eastern Virginia Medical School, Norfolk 23501.
Neurosci Lett. 1993 Apr 30;153(2):121-4. doi: 10.1016/0304-3940(93)90303-3.
Our previous studies have shown that nitric oxide synthase (NOS) can be induced in motoneurons after spinal root avulsion lesion and the lesion-induced NOS is coincident with the death of the injured neurons. The present study examined whether the death of injured motoneurons can be prevented by inhibition of NOS. Nitroarginine, a specific inhibitor of NOS, was injected into adult rats which underwent spinal root avulsion. At a dose of 50 mg/kg/day, nitroarginine significantly inhibited the activity of lesion-induced NOS and significantly reduced the death of motoneurons due to spinal root avulsion. Results of the present study indicate that NO, produced by lesion-induced NOS, may be involved in and responsible for the neuronal death after traumatic injury.
我们之前的研究表明，脊髓神经根撕脱损伤后运动神经元中可诱导产生一氧化氮合酶（NOS），且损伤诱导的NOS与受损神经元的死亡同时出现。本研究检测了通过抑制NOS是否能够预防受损运动神经元的死亡。将NOS的特异性抑制剂硝基精氨酸注射到接受脊髓神经根撕脱术的成年大鼠体内。以50毫克/千克/天的剂量，硝基精氨酸显著抑制损伤诱导的NOS活性，并显著减少因脊髓神经根撕脱导致的运动神经元死亡。本研究结果表明，损伤诱导的NOS产生的NO可能参与并导致创伤性损伤后的神经元死亡。
