Tao Yang1, Bin Kong1, Yongqin Kuang2, Lin Cheng2, Jianwen Gu2, Junhai Zhang2, Haifeng Shu2, Sixun Yu2, Xiaokun Yang3, Jingming Cheng2, Haidong Huang2. 1. Department of Neurosurgery, Chengdu Military General Hospital Chengdu 610083, China ; Department of Neurosurgery, Third Military Medical University Chongqing 400037, China. 2. Department of Neurosurgery, Chengdu Military General Hospital Chengdu 610083, China. 3. Department of Neurosurgery, Third Military Medical University Chongqing 400037, China ; Department of Emergency, Chengdu Military General Hospital Chengdu 610083, China.
Abstract
OBJECTIVE: To observe the interventional effects of emodin in epileptic rats and elucidate its possible mechanism of action. METHODS: Thirty-six female Wistar rats were randomly divided into normal control group, model group (intraperitoneal injection of kainic acid) and emodin group (intraperitoneal injection of kainic acid+emodin intervention). The rat epilepsy model was confirmed by behavioral tests and electroencephalography. The protein levels of P-glycoprotein and N-methyl-D-aspartate (NMDA) receptor in cerebral vascular tissue were analyzed by western blotting, and mRNA levels of multidrug resistance gene 1 (MDR1) and cyclooxygenase-2 (COX-2) were analyzed by real-time PCR. COX-2 and P-glycoprotein levels in the brains were detected by immunohistochemical assay. RESULTS: The seizures were relieved in emodin group. Laser scanning confocal microscopy showed P-glycoprotein fluorescence increased significantly after seizures, indicating that epilepsy can induce overexpression of P-glycoprotein. Compared with control group, protein levels of P-glycoprotein and NMDA receptor in cerebral vascular tissue were significantly higher in model group, and mRNA levels of MDR1 and COX-2 were also significantly increased. Compared with model group, P-glycoprotein and NMDA receptor levels in cerebral vascular tissue were significantly decreased in emodin group (P<0.05), and the levels of MDR1 and COX-2 were down-regulated (P<0.05). In the rat brain, seizures could significantly increase COX-2 and P-glycoprotein levels, while emodin intervention was able to significantly reduce the levels of both. DISCUSSION: These findings suggest that epileptic seizures are tightly associated with up-regulated MDR1 gene, and emodin shows good antagonistic effects on epileptic rats, possibly through inhibition of MDR1 gene and its associated genes.
OBJECTIVE: To observe the interventional effects of emodin in epilepticrats and elucidate its possible mechanism of action. METHODS: Thirty-six female Wistar rats were randomly divided into normal control group, model group (intraperitoneal injection of kainic acid) and emodin group (intraperitoneal injection of kainic acid+emodin intervention). The ratepilepsy model was confirmed by behavioral tests and electroencephalography. The protein levels of P-glycoprotein and N-methyl-D-aspartate (NMDA) receptor in cerebral vascular tissue were analyzed by western blotting, and mRNA levels of multidrug resistance gene 1 (MDR1) and cyclooxygenase-2 (COX-2) were analyzed by real-time PCR. COX-2 and P-glycoprotein levels in the brains were detected by immunohistochemical assay. RESULTS: The seizures were relieved in emodin group. Laser scanning confocal microscopy showed P-glycoprotein fluorescence increased significantly after seizures, indicating that epilepsy can induce overexpression of P-glycoprotein. Compared with control group, protein levels of P-glycoprotein and NMDA receptor in cerebral vascular tissue were significantly higher in model group, and mRNA levels of MDR1 and COX-2 were also significantly increased. Compared with model group, P-glycoprotein and NMDA receptor levels in cerebral vascular tissue were significantly decreased in emodin group (P<0.05), and the levels of MDR1 and COX-2 were down-regulated (P<0.05). In the rat brain, seizures could significantly increase COX-2 and P-glycoprotein levels, while emodin intervention was able to significantly reduce the levels of both. DISCUSSION: These findings suggest that epilepticseizures are tightly associated with up-regulated MDR1 gene, and emodin shows good antagonistic effects on epilepticrats, possibly through inhibition of MDR1 gene and its associated genes.
Authors: Dale C Hesdorffer; Vicki Beck; Charles E Begley; Malachy L Bishop; Sandra Cushner-Weinstein; Gregory L Holmes; Patricia O Shafer; Joseph I Sirven; Joan K Austin Journal: Epilepsia Date: 2013-01-07 Impact factor: 5.864
Authors: A Das; G C Wallace; C Holmes; M L McDowell; J A Smith; J D Marshall; L Bonilha; J C Edwards; S S Glazier; S K Ray; N L Banik Journal: Neuroscience Date: 2012-06-12 Impact factor: 3.590