Delayed acetyl-L-carnitine administration and its effect on sensory neuronal rescue after peripheral nerve injury
Delayed acetyl-L-carnitine administration and its effect on sensory neuronal rescue after peripheral nerve injury
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DOI：
10.1016/j.bjps.2006.04.017
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发表时间：
2007-01-01
影响因子：
2.7
通讯作者：
Terenghi, Giorgio
中科院分区：
文献类型：
--
作者：
Wilson, Andrew D. H.;Hart, Andrew;Terenghi, Giorgio
周围神经损伤后感觉神经元的保护在临床上至关重要。因为高达 40% 的感觉神经元死亡会严重影响感觉恢复不足。立即乙酰左旋肉碱 (ALCAR) 治疗可以消除这种细胞。损失，但可能并不总是在临床上可行，因此我们研究了延迟开始 ALCAR 治疗的效果。五组大鼠（每组 n = 5）接受单侧坐骨神经轴索切断术。受伤后立即开始或延迟 6 小时、24 小时或 7 天后开始 ALCAR 治疗（50 mg/kg/天）。假治疗组作为对照组。损伤和体视学后 2 周收获双侧 L4 和 L5 背根神经节。获得感觉神经元计数。立即假治疗没有提供神经保护（损失25%）。当 ALCAR 开始使用时，细胞损失被消除
Protection of sensory neurons after peripheral nerve injury is clinically crucial. since inadequate sensory recovery is seriously affected by the death of up to 40% of sensory neurons. Immediate acetyl-L-carnitine (ALCAR) treatment eliminates this cell. loss, but may not always be clinically feasible, hence we studied the effect of delaying the initiation of ALCAR treatment.Five groups of rats (n = 5 per group) underwent unilateral sciatic nerve axotomy. ALCAR treatment (50 mg/kg/day) was initiated immediately, or after delays of 6 h, 24 h or 7 days after injury. A sham-treated group served as control. L4 and L5 dorsal root ganglia were harvested bilaterally 2 weeks after injury and stereological. sensory neuron counts were obtained.Immediate sham treatment provided no neuroprotection (25% loss). Cell loss was eliminated when ALCAR was commenced within