天然抗氧化剂减少神经根撕脱诱导的一氧化氮合酶表达和运动神经元死亡

为了研究抗老年性痴呆 990 1号和 TA990 1+银杏叶标准提取物合剂对臂丛神经根撕脱后前角运动神经元的神经元型一氧化氮合酶 ( n NOS)表达和存活的影响 ,用成年 SD雌性大鼠进行右侧臂丛 C5～ T1 神经根撕脱术后 ,随机分为撕脱组、撕脱 +TA990 1组以及撕脱 +TA990 1和 EGb761合剂组。对此三组每天分别进行腹腔注射 1ml生理盐水、0 .5 % TA990 1、0 .5 %TA990 1和 EGb761合剂。治疗 5 d、1、2、4和 6周后处死动物并进行 NADPH-d染色及中性红复染。定量比较各组 n NOS阳性和存活的运动神经元数量。结果证明 ,神经根撕脱后 5 d受损运动神经元开始表达 n NOS,2周时达高峰 ,随后下降至 6周。受损运动神经元的死亡从 2周开始 ,4～ 6周最明显。抗氧化剂治疗组 n NOS表达规律与对照组相似 ,但是阳性程度和阳性细胞数量均少于对照组 ,存活的运动神经元数量则明显多于对照组。撕脱后 4～ 6周 ,TA990 1治疗组抑制 n NOS表达和提高运动神经元存活的效果均明显优于 TA990 1和 EGb761合剂组。结论 :天然抗氧化剂可有效地减少臂丛神经根撕脱后 n NOS表达 ,提高受损运动神经元的存活。 TA990 1抑制 n NOS表达的作用强于 EGb761。

NATURAL ANTIOXIDANTS DECREASE AVULSION-INDUCED NOS EXPRESSION AND MOTONEURONS DEATH FOLLOWING BRACHIAL ROOTS AVULSION

To study the effect of natural antioxidants TA9901 (anti-Alzheimer 9901) and TA9901 plus EGb761 (extract of Ginkgo biloba 761) on nNOS (neuronal nitric oxide synthase) expression and motoneuron death following brachial roots avulsion, adult female Sprague-Dawley rats were randomly divided into avulsion, TA9901 (avulsion plus TA9901), and TA9901 & EGb761 (avulsion plus TA9901 & EGb761) groups. The right C 5～8 , and T 1 nerve roots were avulsed under operating microscope. Everyday after avulsion, the intraperitoneal injection of 1 ml of normal saline, 0.5% TA9901, or 0.5% TA9901 & EGb761 was given to rats in three different groups respectively. The rats were killed after survival for 5 d, 1, 2, 4 and 6 w following the treatments. The cryostat sections of C 7 segments of every rat were carried with NADPH-d (Nicotinamide adenine dinucleotide phosphate diaphorase) histochemistry plus neutral red stain. The numbers of nNOS-positive and survival motoneurons in lesion side of C 7 anterior horn were counted and compared among three groups at each time point. The nNOS was only induced in avulsed motoneurons. In avulsion rats, the nNOS expression in lesioned motoneurons began at 5d, reached peak at 2 w, declined to 6 w following avulsion. The motoneuron death occurred 2 w following avulsion. The death peak appeared 4 to 6 w following avulsion. In TA9901 and TA9901 & EGb761 treated rats, the time course of either nNOS expression or motoneuron death was similar to that of avulsion rats. But the number of nNOS-positive motoneurons was significantly less than that of avulsion rats. The survival motoneurons in avulsion group were significantly less than that in TA9901 group from 2 w to 6 w and in TA9901 & EGb761 group only at 2 w. Both nNOS-positive and survival motoneurons in TA9901 group were less than those in TA9901 & EGb761 group at 4 w and 6 w following avulsion. Our results indicate that natural antioxidants can reduce avulsion-induced motoneuron nNOS expression and motoneuron death. TA9901 was more powerful than EGb761 in inhibition of motoneuron nNOS expression following brachial roots avulsion.