PDF(Pubmed)
Abstract：
UNASSIGNED: Epilepsy is a serious mental disease, for which oxidative stress and hippocampal neuron death after seizure is crucial. Numerous miRNAs are involved in epilepsy. However, the function of miR-98-5p in oxidative stress and hippocampal neuron death after seizure is unclear, which is the purpose of current study.
UNASSIGNED: Magnesium ion (Mg2+)-free solution was used to establish the in vitro epilepsy model in hippocampal neurons. Oxidative stress was exhibited by measuring malondialdehyde (MDA) level and superoxide Dismutase (SOD) activity using enzyme-linked immune sorbent assay (ELISA) kits. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were applied for the examination of neuron viability and apoptosis, respectively. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot were used to evaluate the mRNA and protein levels of miR-98-5p and signal transducer and activator of transcription (STAT3), respectively. The relationship between miR-98-5p and STAT3 was predicted by TargetScan 7.2, and identified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
UNASSIGNED: miR-98-5p was decreased in the in vitro epileptic model of hippocampal neurons induced by Mg2+-free solution, whose overexpression rescued oxidative stress and neuron apoptosis in epileptic model. Moreover, overexpression of STAT3, one downstream target of miR-98-5p, partially eliminated the effects of miR-98-5p mimic.
UNASSIGNED: We shed lights on a pivotal mechanism of miR-98-5p in regulating neuron oxidative stress and apoptosis after seizures, providing potential biomarkers for the diagnosis of epilepsy and therapeutic targets for the treatment of epilepsy.
UNASSIGNED: Magnesium ion (Mg2+)-free solution was used to establish the in vitro epilepsy model in hippocampal neurons. Oxidative stress was exhibited by measuring malondialdehyde (MDA) level and superoxide Dismutase (SOD) activity using enzyme-linked immune sorbent assay (ELISA) kits. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were applied for the examination of neuron viability and apoptosis, respectively. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot were used to evaluate the mRNA and protein levels of miR-98-5p and signal transducer and activator of transcription (STAT3), respectively. The relationship between miR-98-5p and STAT3 was predicted by TargetScan 7.2, and identified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
UNASSIGNED: miR-98-5p was decreased in the in vitro epileptic model of hippocampal neurons induced by Mg2+-free solution, whose overexpression rescued oxidative stress and neuron apoptosis in epileptic model. Moreover, overexpression of STAT3, one downstream target of miR-98-5p, partially eliminated the effects of miR-98-5p mimic.
UNASSIGNED: We shed lights on a pivotal mechanism of miR-98-5p in regulating neuron oxidative stress and apoptosis after seizures, providing potential biomarkers for the diagnosis of epilepsy and therapeutic targets for the treatment of epilepsy.
摘要：
■癫痫是一种严重的精神疾病,对于癫痫发作后的氧化应激和海马神经元死亡至关重要。许多miRNA与癫痫有关。然而,miR-98-5p在惊厥后氧化应激和海马神经元死亡中的作用尚不清楚,这是当前研究的目的。
■采用无镁离子(Mg2+)溶液建立海马神经元体外癫痫模型。通过使用酶联免疫吸附测定（ELISA）试剂盒测量丙二醛（MDA）水平和超氧化物歧化酶（SOD）活性来显示氧化应激。应用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)法和流式细胞术检测神经元活力和凋亡,分别。定量逆转录聚合酶链反应（qRT-PCR）和Westernblot用于评估miR-98-5p和信号转导和转录激活因子（STAT3）的mRNA和蛋白水平。分别。通过TargetScan7.2预测miR-98-5p与STAT3之间的关系，并通过双荧光素酶报告基因测定和RNA免疫沉淀（RIP）测定进行鉴定。
■miR-98-5p在无Mg2+溶液诱导的海马神经元体外癫痫模型中降低，其过度表达在癫痫模型中拯救了氧化应激和神经元凋亡。此外，过表达STAT3，miR-98-5p的一个下游靶标，部分消除了miR-98-5p模拟物的影响。
■我们揭示了miR-98-5p在癫痫发作后调节神经元氧化应激和凋亡的关键机制，为癫痫的诊断和治疗提供潜在的生物标志物。
■采用无镁离子(Mg2+)溶液建立海马神经元体外癫痫模型。通过使用酶联免疫吸附测定（ELISA）试剂盒测量丙二醛（MDA）水平和超氧化物歧化酶（SOD）活性来显示氧化应激。应用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)法和流式细胞术检测神经元活力和凋亡,分别。定量逆转录聚合酶链反应（qRT-PCR）和Westernblot用于评估miR-98-5p和信号转导和转录激活因子（STAT3）的mRNA和蛋白水平。分别。通过TargetScan7.2预测miR-98-5p与STAT3之间的关系，并通过双荧光素酶报告基因测定和RNA免疫沉淀（RIP）测定进行鉴定。
■miR-98-5p在无Mg2+溶液诱导的海马神经元体外癫痫模型中降低，其过度表达在癫痫模型中拯救了氧化应激和神经元凋亡。此外，过表达STAT3，miR-98-5p的一个下游靶标，部分消除了miR-98-5p模拟物的影响。
■我们揭示了miR-98-5p在癫痫发作后调节神经元氧化应激和凋亡的关键机制，为癫痫的诊断和治疗提供潜在的生物标志物。
