目的 检测大鼠神经根慢性损伤后脊髓神经细胞的凋亡率,同时探讨不同类型非甾体抗炎药(NSAIDs)对此的影响,试图解释腰椎管狭窄症的一些不典型症状.方法 将48只SD大鼠随机分为对照组、结扎组、吲哚美辛组和美洛昔康组各12只.在结扎组、吲哚美辛组和美洛昔康组,造成神经根慢性压迫性损伤模型,后2组术后分别喂服吲哚美辛、美洛昔康,饲养4周处死,提取标本.结果 在结扎组,凋亡指数与神经损伤评分之间存在正相关(r=0.858,P0.05),与结扎组比较均有非常显著差异(P0.05).免疫组化法显示结扎组Bax蛋白表达与各组比较均有非常显著差异(P0.05).结论 神经根慢性压迫性损伤可以引起相应脊髓节段前角运动神经元的凋亡,与损伤程度正相关;非选择性环氧化酶(COX)抑制剂吲哚美辛和选择性COX-2抑制剂美洛昔康均可抑制脊髓神经细胞的凋亡;但未明显改善大鼠的神经损伤症状.%Objective To explore the apoptosis of nerve cells in spinal cord of rats induced by chronic nerve root injury, and to study the influence by different types of JNSAlDs, and to try to explain some atypical symptoms in patients with lumbar spinal stenosis syndrome. Methods Forty eight SD rats were allocated into four groups: control group, ligation group, indometacin group and meloxicam group, each group with 12 rats. The model of chronic compressive injury of spinal nerve had been established in rats. Rats in indometacin group and meloxicam group were fed with indometacin and meloxicam respectively after surgery. Rats were killed after 4 weeks for examination. Results There was positive correlation between apoptotic index and nerve injury scores ( r - 0. 0858 , P 0. 05 ), but there was significant difference between these two groups with ligation group ( P 0.05 ). The results of immunohistochemical method demonstrated that a little expression of bcl - 2 and Bax proteins was presented in rats of control group, significantly increased expression of Bax protein and no expression of bcl - 2 protein in ligation group, a little expression of bcl - 2 and Bax proteins in indometacin and meloxicam groups. Conclusion The chronic compressive injury of nerve root can cause apoptosis of motor neurons in anterior angle of spinal cord connected to nerve root, and there was positive correlation with the degree of injury. JNonselective COX inhibitor - indometacin and selective COX - 2 inhibitor - meloxicam both can prevent the apoptosis of spinal nerve cells. These results indicated that mechanism of inhibiting apoptosis of nerve cells by JNSAlDs is independent to isomer of COX; and JNSAlDs dont improve symptoms of nerve injury in rats.
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