石菖蒲挥发油对氯化锂-匹鲁卡品致痫大鼠血清和脑脊液CGRP及NSE表达的影响

Effects of volatile oils from Rhizoma Acori Tatarinowii on expressions of CGRP and NSE in serum and cerebrospinal fluid of lithium chloride- pilocarpine induced epileptic rats

目的:探讨石菖蒲挥发油对氯化锂-匹鲁卡品致痫大鼠血清和脑脊液中降钙素基因相关肽(CGRP)及神经元特异性烯醇化酶(NSE)表达的影响。方法:依照随机数字原则将成年雄性SD大鼠66只,分为对照组(6只)、癫痫组(30只)、石菖蒲挥发油组(30只),后两组采用氯化锂-匹鲁卡品灌胃法建立癫痫动物模型。在痫性发作后6h、12h、24h抽取血液和脑脊液,用ELISA方法测定血清及脑脊液中CGRP和NSE含量。结果:癫痫组与石菖蒲挥发油组大鼠血清和脑脊液中CGRP含量在致痫后6h开始上升,24h达到最大值。两组血清和脑脊液中CGRP含量在相同时间点存在显著差异(P<0.05),两组CGRP含量在相同时间点均低于对照组,差异有统计学意义(P<0.05);癫痫组与石菖蒲挥发油组大鼠血清和脑脊液中NSE的浓度在致痫后6h数值最高,12h-24h逐渐下降。两组血清和脑脊液中NSE含量在相同时间点相比存在显著差异(P<0.05),两组血清NSE含量在相同时间点均高于对照组,差异有统计学意义(P<0.05)。结论:血清和脑脊液中CGRP与NSE表达水平的变化是癫痫后脑损伤的早期生化指标,石菖蒲挥发油可能是通过降低血清及脑脊液中NSE的表达、升高CGRP的表达,而减少神经元的损伤,达到对致痫后大鼠脑神经元的保护作用。

Objective： To investigate the effects of volatile oils from Rhizoma Acori Tatarinowii on the expression of ealcitonin gene -related peptide （CGRP） and neuron - specific enolase （NSE） in serum and cerebrospinal fluid of lithium chloride -pilocarpine induced epileptic rats. Methods： The 66 adult male SD rats were grouped into the control group （ n = 6）, epilepsy group （ n = 30） and volatile oil group （n =0 ） according to the principle of random numbers. Lithium chloride -piloearpine was given by gavage to the rats in the latter 2 groups to establish epilepsy models. Blood and cerebrospinal fluid samples were obtained 6h, 12h and 24h after epileptic seizure, followed by detection of CGRP and NSE levels in serum and eerebrospinal fluid by ELISA. Results： The CGRP levels in the serum and cerebrospinal fluid of the epilepsy group and vola- tile oil group started to increase 6h after epileptic seizure, and reached the peak at 12 -24h after epileptic sei- zure, but started to decrease at 72h. The difference in the CGRP levels at the same time point between the two groups was statistically significant （P 〈 0. 05 ）. Besides, the CGRP levels in these 2 groups were lower than those in the eontrol group at the same time point, and the difference was statistically significant （ P 〈 0. 05 ）. In epilepsy group and volatile oil group, the serum and erebrospinal fluid levels of NSE started to decrease 6h after epileptic seizure, and reached the lowest at 24h. But the NSE levels at the same time point differed significantly between the two groups （ P 〈 0. 05 ）. The serum and erebrospinal fluid levels of NSE in the epilepsy group and volatile oil group were significantly higher compared to those in the control group （P 〈 0. 05 ）. Conclusion： Variances in expression levels of CGRP and NSE in serum and cerebrospinal fluid were the early biochemical indicators for brain injury after epileptic seizure. Volatile Oils from Rhizoma Acori Tatarinowii could reduce neural damage and prevent brain neurons from the damage of epileptic seizure by down - regulating expression of NES and up -regulating expression of CGRP in serum and cerebrospinal fluid.