PDF(Pubmed)
Abstract：
UNASSIGNED: Transient receptor potential (TRP) channels have been found to have significant implications in neuronal outgrowth, survival, inflammatory neurogenic pain, and various epileptogenic processes. Moreover, there is a growing body of evidence indicating that transient receptor potential (TRP) channels have a significant impact on epilepsy and its drug-resistant subtypes.
UNASSIGNED: We postulated that EGb 761 would modulate TRPA1 channels, thereby exhibiting anti-inflammatory and neuroprotective effects in a neuroblastoma cell line. Our rationale was to investigate the impact of EGb 761 in a controlled model of pentylenetetrazole-induced generalized epilepsy.
UNASSIGNED: We evaluated the neuroprotective, antioxidant and anti-apoptotic effects of EGb 761 both before and after the pentylenetetrazole application in a neuroblastoma cell line. Specifically, we focused on the effects of EGB 761 on the activity of Transient receptor potential (TRP) channels.
UNASSIGNED: EGb 761 applications both before and after the pentylenetetrazole incubation period reduced Ca release and restored apoptosis, ROS changes, mitochondrial depolarization and caspase levels, suggesting a prominent prophylactic and therapeutic effect of EGb 761 in the pentylenetetrazole-induced epileptogenesis process.
UNASSIGNED: Our basic mechanistic framework for elucidating the pathophysiological significance of fundamental ion mechanisms in a pentylenetetrazole treated neuroblastoma cell line provided compelling evidence for the favorable efficacy and safety profile of Egb 761 in human-relevant in vitro model of epilepsy. To the best of our knowledge, this is the first study to investigate the combined effects of EGb 761 and pentylenetetrazole on TRP channels and measure their activation level in a relevant model of human epileptic diseases.
UNASSIGNED: We postulated that EGb 761 would modulate TRPA1 channels, thereby exhibiting anti-inflammatory and neuroprotective effects in a neuroblastoma cell line. Our rationale was to investigate the impact of EGb 761 in a controlled model of pentylenetetrazole-induced generalized epilepsy.
UNASSIGNED: We evaluated the neuroprotective, antioxidant and anti-apoptotic effects of EGb 761 both before and after the pentylenetetrazole application in a neuroblastoma cell line. Specifically, we focused on the effects of EGB 761 on the activity of Transient receptor potential (TRP) channels.
UNASSIGNED: EGb 761 applications both before and after the pentylenetetrazole incubation period reduced Ca release and restored apoptosis, ROS changes, mitochondrial depolarization and caspase levels, suggesting a prominent prophylactic and therapeutic effect of EGb 761 in the pentylenetetrazole-induced epileptogenesis process.
UNASSIGNED: Our basic mechanistic framework for elucidating the pathophysiological significance of fundamental ion mechanisms in a pentylenetetrazole treated neuroblastoma cell line provided compelling evidence for the favorable efficacy and safety profile of Egb 761 in human-relevant in vitro model of epilepsy. To the best of our knowledge, this is the first study to investigate the combined effects of EGb 761 and pentylenetetrazole on TRP channels and measure their activation level in a relevant model of human epileptic diseases.
摘要：
■已经发现瞬时受体电位（TRP）通道在神经元生长中具有重要意义，生存,炎性神经源性疼痛，和各种癫痫过程。此外，越来越多的证据表明瞬时受体电位(TRP)通道对癫痫及其耐药亚型有显著影响.
■我们假设EGb761会调制TRPA1通道，从而在神经母细胞瘤细胞系中表现出抗炎和神经保护作用。我们的理由是研究EGb761在戊四氮诱导的全身性癫痫的对照模型中的影响。
■我们评估了神经保护作用，EGb761在神经母细胞瘤细胞系中应用戊四氮前后的抗氧化和抗凋亡作用。具体来说,我们重点研究了EGB761对瞬时受体电位（TRP）通道活性的影响。
■戊四唑潜伏期前后应用EGb761可减少Ca释放并恢复细胞凋亡，ROS的变化，线粒体去极化和半胱天冬酶水平，提示EGb761在戊四唑诱导的癫痫发生过程中具有突出的预防和治疗作用。
■我们阐明戊四唑治疗的神经母细胞瘤细胞系中基本离子机制的病理生理学意义的基本机制框架为Egb761在人类相关的体外癫痫模型中的良好疗效和安全性提供了令人信服的证据。据我们所知,这是第一项研究EGb761和戊四唑对TRP通道的联合作用,并在相关的人类癫痫疾病模型中测量它们的激活水平.
■我们假设EGb761会调制TRPA1通道，从而在神经母细胞瘤细胞系中表现出抗炎和神经保护作用。我们的理由是研究EGb761在戊四氮诱导的全身性癫痫的对照模型中的影响。
■我们评估了神经保护作用，EGb761在神经母细胞瘤细胞系中应用戊四氮前后的抗氧化和抗凋亡作用。具体来说,我们重点研究了EGB761对瞬时受体电位（TRP）通道活性的影响。
■戊四唑潜伏期前后应用EGb761可减少Ca释放并恢复细胞凋亡，ROS的变化，线粒体去极化和半胱天冬酶水平，提示EGb761在戊四唑诱导的癫痫发生过程中具有突出的预防和治疗作用。
■我们阐明戊四唑治疗的神经母细胞瘤细胞系中基本离子机制的病理生理学意义的基本机制框架为Egb761在人类相关的体外癫痫模型中的良好疗效和安全性提供了令人信服的证据。据我们所知,这是第一项研究EGb761和戊四唑对TRP通道的联合作用,并在相关的人类癫痫疾病模型中测量它们的激活水平.
