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1.
J Mol Neurosci ; 65(2): 234-245, 2018 Jun.
Article in English | MEDLINE | ID: mdl-29858824

ABSTRACT

Epilepsy is a common chronic brain disorder and is characterized by an enduring predisposition to generate seizures. The hippocampus is especially vulnerable to seizure-induced damage. In this study, we explore the ability of long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) to influence the autophagy and apoptosis of hippocampal neurons in epilepsy and the underlying mechanism involving the PI3K/Akt signaling pathway. Seventy-two Sprague-Dawley rats were assigned to normal, sham, Ep, Ep + si-NC, Ep + si-MALAT1, and Ep + si-MALAT1 + LY groups. Fluorescence in situ hybridization kit was employed to determine the MALAT1 in the brain tissues. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were performed to determine the expression of MALAT1, mRNAs, and proteins. The autophagy of hippocampal neurons was evaluated under a transmission electron microscope and their apoptosis was evaluated using TUNEL staining. We found that MALAT1 and c-Met were enriched while microRNA-101 (miR-101) decreased in rats with epilepsy. The demonstration showed that MALAT1 binds to miR-101, thus regulating c-Met. In rats with epilepsy, MALAT1 depletion mediated by anti-MALAT1 siRNA resulted in activation of PI3K/Akt signaling pathway and loss of hippocampal neurons. LY294002, an inhibitor of PI3K/Akt signaling pathway, could reverse the events caused by MALAT1 knockdown. Taken together, these findings indicate that down-regulation of MALAT1 activates the PI3K/Akt signaling pathway to protect hippocampal neurons against autophagy and apoptosis in rats with epilepsy.


Subject(s)
Apoptosis , Autophagy , Down-Regulation , Epilepsy/metabolism , Hippocampus/metabolism , RNA, Long Noncoding/genetics , Signal Transduction , Animals , Epilepsy/genetics , Hippocampus/cytology , Neurons/metabolism , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , RNA, Long Noncoding/metabolism , Rats , Rats, Sprague-Dawley
2.
Pak J Pharm Sci ; 29(6 Suppl): 2317-2320, 2016 Nov.
Article in English | MEDLINE | ID: mdl-28167472

ABSTRACT

To explore the relationship between the clinical manifestations and functional magnetic resonance images of delayed encephalopathy after carbon monoxide intoxication. Six patients received the MRI were diagnosed with delayed encephalopathy after carbon monoxide (CO) poisoning. Clinical manifestations were observed in each patient. MRI revealed multiple lesions. The majority of the lesions were located in the globus pallidus, sub cortical white matter, and basal ganglia. The cognitive injury, akinetic mutism, fecal and uroclepsia, forced crying, forced laughing and extra pyramidal syndromes such as chorea and parkinsonism were manifested in clinic. Cognitive impairment improved greatly while involuntary movements only improved slightly after several months. Meanwhile brain MRI suggested remarkable improvement. Neuroimaging directly correlated with the clinical manifestations.


Subject(s)
Brain Diseases/diagnostic imaging , Brain/diagnostic imaging , Carbon Monoxide Poisoning/diagnostic imaging , Cognition Disorders/diagnostic imaging , Cognition , Functional Neuroimaging/methods , Magnetic Resonance Imaging , Aged , Brain Diseases/chemically induced , Brain Diseases/physiopathology , Brain Diseases/psychology , Carbon Monoxide Poisoning/complications , Carbon Monoxide Poisoning/physiopathology , Carbon Monoxide Poisoning/psychology , China , Cognition Disorders/chemically induced , Cognition Disorders/physiopathology , Cognition Disorders/psychology , Dyskinesia, Drug-Induced/diagnostic imaging , Dyskinesia, Drug-Induced/etiology , Dyskinesia, Drug-Induced/physiopathology , Dyskinesia, Drug-Induced/psychology , Female , Humans , Male , Middle Aged , Predictive Value of Tests , Prognosis , Recovery of Function , Retrospective Studies , Time Factors
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