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目的探讨神经元特异性烯醇化酶(Neuron Specific Enolase,简称NSE)、星形胶质源性蛋白(S-100βprotein,简称S-100β)和环氧化酶-2(Cyclooxygenase-2,简称COX-2)在1-溴丙烷大鼠亚急性神经损伤中的变化。方法选取健康雄性Wistar大鼠36只,随机分为0ppm(对照组)和1000ppm1-BP染毒组,每组18只,采用口鼻吸入染毒方法,每天染毒6h连续染毒21d。染毒期间隔天称量并记录动物体重,于染毒后第七、十四和二十一天分批次各处死6只动物,采集脑组织和血液(分离血清),每组2只动物分离大脑、垂体、脊髓、坐骨神经和胫腓神经用于病理检测。用ELISA试剂盒检测大鼠脑组织和血清中NSE,S-100β,COX-2等指标的变化。结果与对照组相比,1000ppm染毒21d的染毒组动物体重增长明显减慢(P<0.05),病理检查可见小脑局部浦肯野细胞萎缩、腰髓灰质空泡变性、胫腓神经部分神经纤维肿胀增粗;在染毒的第一周和第三周,大鼠脑组织中NSE、S-100β和COX-2等神经损伤特异性指标与对照组相比显著增高(P<0.05),血清中NSE在第三周有升高趋势,但与对照组相比差异不显著;S-100β在第三周显著增高(P<0.05);而COX-2在前2周显著增高(P<0.05),第三周与对照组差异不显著;脑组织和血清中S-100β的变化显著相关。结论综合实验动物脑组织和血清中神经特异性损伤指标(NSE、S-100β和COX-2)的变化以及病理检查结果,1-BP大鼠染毒模型可以在现有的试验条件和染毒条件下,引起实验动物的亚急性神经损伤。
Objective To investigate the expression of neuron specific enolase (NSE), S-100βprotein (S-100β) and cyclooxygenase-2 (COX- 2) Changes in Subacute Nerve Injury in 1-Bromopropane-induced Rats. Methods Thirty-six healthy male Wistar rats were randomly divided into 0 ppm (control group) and 1000 ppm 1-BP group (n = 18). The rats were treated with oral and nasal inhalation. Body weight was weighed and recorded every other day during the exposure period. Six animals were sacrificed in batches on the seventh, fourteenth and twenty-one days after the exposure. Cerebral tissues and blood (serums were separated), two animals in each group Separation of the brain, pituitary, spinal cord, sciatic nerve and tibiofibular nerve for pathological detection. The changes of NSE, S-100β and COX-2 in rat brain and serum were detected by ELISA kit. Results Compared with the control group, the weight gain of rats exposed to 1000ppm for 21d was significantly slower than that of the control group (P <0.05). Pathological examination revealed atrophy of Purkinje cells in the cerebellum, degeneration of gray matter in the spinal cord, In the first week and the third week of exposure, the specific indexes of nerve injury such as NSE, S-100β and COX-2 in rat brain tissue were significantly higher than those in control group (P <0.05) The level of NSE in serum increased in the third week, but not significantly different from that in the control group (P <0.05) , There was no significant difference between the third week and the control group; the change of S-100β in the brain tissue and the serum was significantly correlated. Conclusion The changes of neuron specific damage index (NSE, S-100β and COX-2) in brain tissue and serum of experimental animals and the results of pathological examination show that the model of 1-BP rat exposure can be established under the existing experimental conditions and exposure Under conditions, causing subacute nerve injury in experimental animals.