天浆牛黄散对匹罗卡品大鼠癫痫模型的影响
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摘要
目的观察天浆牛黄散对匹罗卡品大鼠癫痫模型认知、癫痫发作、海马结构的影响。方法 SD大鼠40只,随机分为4组(n=10),分别为空白对照组(A组)和3个匹罗卡品大鼠癫痫模型组,模型组按照不同的处理方式分为:天浆牛黄散治疗组(B组)、丙戊酸钠组(C组)和模型对照组(D组)。观察第7、14、21 d大鼠癫痫发作情况、脑电图监测大鼠放电次数、认知能力;大鼠处死后行脑组织病理切片检测,观察海马CA1区神经元损伤。结果 B组与C组大鼠癫痫自发性发作次数、持续时间、每分钟平均放电次数均无统计学差异(P>0.05);D组与B、C组相比,发作次数增多、持续时间增长、放电次数增多,差异具有统计学意义(P<0.05);A组大鼠无癫痫发作。大鼠在认知能力方面,A、B与C组比较均无统计学差异(P>0.05),D组与A、B、C组相比,认知能力较差(P<0.05);大鼠海马区CA1区存活细胞数,B、C与D组相比有明显改善(P<0.05);与A组相比3个实验组海马CA1区存活细胞显著降低(P<0.05)。结论天浆牛黄散能减少匹罗卡品大鼠癫痫模型的癫痫发作、改善认知、有效减轻癫痫发作和海马CA1区神经元的损伤。
Objective To observe the effects of Tianjiang Niuhuang Powder on cognition, seizure and hippocampal formation in epileptic model of pilocarpine rats. Methods Fouty SD rats were selected in this study. They were randomly divided into four groups(each group n=10), including a blank control group(group A) and three pilocarpine epilepsy model groups. The model groups were divided into Tianjiang Niuhuang Powder treatment Group(group B), Sodium valproate(group C) and model control group(group D) according to the different processing methods.The seizures number of discharges in the EEG monitor, cognitive ability were observed on the 7 th, 14 th and 21 st day, The pathological sections of the brain and the neuronal damage in the hippocampal CA1 area were observed after the rats were sacrificed. Results There was no significant difference in the number of spontaneous episodes, duration, and average number of discharges per minute between group B and group C(P>0.05). Compared with groups B and C, group D increased the number of episodes and increased duration. The number of discharges increased, the difference was statistically significant(P<0.05). Group A had no seizures. There were no significant differences in cognitive ability between groups A, B and C(P>0.05). Compared with group A, B and C, group D had poor cognitive ability(P<0.05). The number of surviving cells in the hippocampus CA1 region was significantly improved compared with the D group(P<0.05). Compared with the A group, the viable cells in the hippocampal CA1 region of the three experimental groups were significantly lower(P<0.05). Conclusions Tianjiang Niuhuang Powder can reduce seizures, improve cognition and effectively alleviate neuronal damage in hippocampal CA1 neurons in rats with epilepsy.
Objective To observe the effects of Tianjiang Niuhuang Powder on cognition, seizure and hippocampal formation in epileptic model of pilocarpine rats. Methods Fouty SD rats were selected in this study. They were randomly divided into four groups(each group n=10), including a blank control group(group A) and three pilocarpine epilepsy model groups. The model groups were divided into Tianjiang Niuhuang Powder treatment Group(group B), Sodium valproate(group C) and model control group(group D) according to the different processing methods.The seizures number of discharges in the EEG monitor, cognitive ability were observed on the 7 th, 14 th and 21 st day, The pathological sections of the brain and the neuronal damage in the hippocampal CA1 area were observed after the rats were sacrificed. Results There was no significant difference in the number of spontaneous episodes, duration, and average number of discharges per minute between group B and group C(P>0.05). Compared with groups B and C, group D increased the number of episodes and increased duration. The number of discharges increased, the difference was statistically significant(P<0.05). Group A had no seizures. There were no significant differences in cognitive ability between groups A, B and C(P>0.05). Compared with group A, B and C, group D had poor cognitive ability(P<0.05). The number of surviving cells in the hippocampus CA1 region was significantly improved compared with the D group(P<0.05). Compared with the A group, the viable cells in the hippocampal CA1 region of the three experimental groups were significantly lower(P<0.05). Conclusions Tianjiang Niuhuang Powder can reduce seizures, improve cognition and effectively alleviate neuronal damage in hippocampal CA1 neurons in rats with epilepsy.
引文
1姚俐.川芎嗪抗小鼠实验性癫痫的研究.广州:南方科技大学,硕士学位论文, 2013.
2洪震.丙戊酸钠--癫痫治疗一线用药.癫痫杂志, 2017, 3(3):278-279.
3Peng WF, Ding J, Li X, et al. N-methyl-d-aspartate receptor NR2B subunit involved in depression-like behaviours in lithium chloride-pilocarpine chronic rat epilepsy model. Epilepsy Res, 2016, 119:77-85.
4Pfammatter JA, Bergstorm RA, Wallace EP, et al. A predictive epilepsy index based on probabilistic classification of interictal spike waveforms. PLoS One, 2018, 13(11):e0207158.
5Loddenkemper T, Talos DM, Cleary RT, et al. Subunit composition of glutamate and gamma-aminobutyric acid receptors in status epilepticus. Epilepsy Res, 2014, 108(4):605-615.
6Ghadiri T, Sharifzadeh M, Khodagholi M, et al. A novel traumatic brain injury model for induction of mild brain injury in rats. J Neurosci Methods, 2014, 233:18-27.
7Wan J, Wan H, Yang R, et al. Protective effect of Dandong Injection combined with Naoxintong Capsule on cerebral ishemiareperfusion injury in rats. J Ethnopharmacol, 2018, 211:348-357.
8Tuor UI, Zhao Z, Barber PA, et al. Recurrent mild cerebral ischemia:enhanced brain injury following acute compared to subacute recurrence in the rat. BWC Neurosci, 2016, 17(1):28.
9 Shih JJ, Whitlock JB, Chimato N, et al. Epilepsy treatment in adults and adolescents:Expert opinion, 2016. Epilepsy Behav, 69:186-
222.10Brodie MJ, Besag F, Ettinger AB, et al. Epilepsy, antiepileptic drugs,and aggression:an evidence-based review. Pharmacological Reviews, 2016, 68(3):563-602.
11L?scher W. Animal models of seizures and epilepsy:past, present,and future role for the discovery of antiseizure drugs. Neurochem Res, 2017, 42(7):1873-1888.
12Butler KM, Moody OA, Elisabeth S, et al. De novo variants in GABRA2 and GABRA5 alter receptor function and contribute to early-onset epilepsy. Brain, 2018, 141(8):2392-2405.
13Murase S. A new model for developmental neuronal death and excitatory/inhibitory balance in hippocampus. Mol Neurobiol,2014, 49(1):316-325.
14Tse MT, Piantadosi PT, Floresco SB. Prefrontal cortical gamma-aminobutyric acid transmission and cognitive function:drawing links to schizophrenia from preclinical research. Biol Psychiatry,2015, 77(11):929-939.
15Kang JQ. Defects at the crossroads of GABAergic signaling in generalized genetic epilepsies. Epilepsy Res, 2017, 137:9-18.
16 Uchida T, Lossin C, Ihara Y, et al. Abnormalγ-aminobutyric acid neurotransmission in a Kcnq2 model of early onset epilepsy.Epilepsia, 2017, 58(8):1430-1439.
2洪震.丙戊酸钠--癫痫治疗一线用药.癫痫杂志, 2017, 3(3):278-279.
3Peng WF, Ding J, Li X, et al. N-methyl-d-aspartate receptor NR2B subunit involved in depression-like behaviours in lithium chloride-pilocarpine chronic rat epilepsy model. Epilepsy Res, 2016, 119:77-85.
4Pfammatter JA, Bergstorm RA, Wallace EP, et al. A predictive epilepsy index based on probabilistic classification of interictal spike waveforms. PLoS One, 2018, 13(11):e0207158.
5Loddenkemper T, Talos DM, Cleary RT, et al. Subunit composition of glutamate and gamma-aminobutyric acid receptors in status epilepticus. Epilepsy Res, 2014, 108(4):605-615.
6Ghadiri T, Sharifzadeh M, Khodagholi M, et al. A novel traumatic brain injury model for induction of mild brain injury in rats. J Neurosci Methods, 2014, 233:18-27.
7Wan J, Wan H, Yang R, et al. Protective effect of Dandong Injection combined with Naoxintong Capsule on cerebral ishemiareperfusion injury in rats. J Ethnopharmacol, 2018, 211:348-357.
8Tuor UI, Zhao Z, Barber PA, et al. Recurrent mild cerebral ischemia:enhanced brain injury following acute compared to subacute recurrence in the rat. BWC Neurosci, 2016, 17(1):28.
9 Shih JJ, Whitlock JB, Chimato N, et al. Epilepsy treatment in adults and adolescents:Expert opinion, 2016. Epilepsy Behav, 69:186-
222.10Brodie MJ, Besag F, Ettinger AB, et al. Epilepsy, antiepileptic drugs,and aggression:an evidence-based review. Pharmacological Reviews, 2016, 68(3):563-602.
11L?scher W. Animal models of seizures and epilepsy:past, present,and future role for the discovery of antiseizure drugs. Neurochem Res, 2017, 42(7):1873-1888.
12Butler KM, Moody OA, Elisabeth S, et al. De novo variants in GABRA2 and GABRA5 alter receptor function and contribute to early-onset epilepsy. Brain, 2018, 141(8):2392-2405.
13Murase S. A new model for developmental neuronal death and excitatory/inhibitory balance in hippocampus. Mol Neurobiol,2014, 49(1):316-325.
14Tse MT, Piantadosi PT, Floresco SB. Prefrontal cortical gamma-aminobutyric acid transmission and cognitive function:drawing links to schizophrenia from preclinical research. Biol Psychiatry,2015, 77(11):929-939.
15Kang JQ. Defects at the crossroads of GABAergic signaling in generalized genetic epilepsies. Epilepsy Res, 2017, 137:9-18.
16 Uchida T, Lossin C, Ihara Y, et al. Abnormalγ-aminobutyric acid neurotransmission in a Kcnq2 model of early onset epilepsy.Epilepsia, 2017, 58(8):1430-1439.