• Publications
  • Influence
Chronic exposure to ethanol of male mice before mating produces attention deficit hyperactivity disorder‐like phenotype along with epigenetic dysregulation of dopamine transporter expression in mouse
TLDR
It is suggested that preconceptional exposure to EtOH through the paternal route induces behavioral changes in offspring, possibly via epigenetic changes in gene expression, which is essential for the regulation of ADHD‐like behaviors. Expand
Male‐specific alteration in excitatory post‐synaptic development and social interaction in pre‐natal valproic acid exposure model of autism spectrum disorder
TLDR
The results suggest that prenatally VPA‐exposed rats show the male preponderance of ASD‐like behaviors including defective social interaction similar to human autistic patients, which might be caused by ectopic increase in glutamatergic synapses in male rats. Expand
Activation of protease-activated receptor1 mediates induction of matrix metalloproteinase-9 by thrombin in rat primary astrocytes
TLDR
The results suggest that the activation of PAR1 mediates thrombin-induced MMP-9 expression through the regulation of Erk1/2. Expand
Pax6-Dependent Cortical Glutamatergic Neuronal Differentiation Regulates Autism-Like Behavior in Prenatally Valproic Acid-Exposed Rat Offspring
TLDR
Together, environmental factors may contribute to the imbalance in excitatory/inhibitory neuronal activity in autistic brain by altering expression of transcription factors governing glutamatergic/GABAergic differentiation during fetal neural development, in conjunction with the genetic preload. Expand
Neuroprotective effects of valproic acid against hemin toxicity: Possible involvement of the down-regulation of heme oxygenase-1 by regulating ubiquitin–proteasomal pathway
TLDR
The results indicate that VPA inhibits hemin toxicity by downregulating HO-1 protein expression, and provide a therapeutic strategy to attenuate intracerebral hemorrhagic injury. Expand
The Epigenetic Reader BRD2 as a Specific Modulator of PAI-1 Expression in Lipopolysaccharide-Stimulated Mouse Primary Astrocytes
TLDR
The data suggest that BRD2 is involved in the modulation of neuroinflammatory responses through PAI-1 and via the regulation of epigenetic reader BET protein, further providing a potential novel therapeutic strategy in neuroinflammatory diseases. Expand
Spinosin, a C-glycoside flavonoid, enhances cognitive performance and adult hippocampal neurogenesis in mice
TLDR
It is demonstrated that spinosin has the potential for therapeutic use in treating the cognitive dysfunction observed in neurological or psychiatric disorders by up-regulating adult hippocampal neurogenesis or activating of the ERK-CREB-BDNF signaling pathway. Expand
Activation of Glucagon-Like Peptide-1 Receptor Promotes Neuroprotection in Experimental Autoimmune Encephalomyelitis by Reducing Neuroinflammatory Responses
TLDR
Exendin-4 administration to symptomatic EAE mice significantly improved the clinical signs of the disease, along with the reversal of histopathological sequelae such as cell accumulation, demyelination, astrogliosis, microglial activation, and morphological transformation of activated microglia in the injured spinal cord. Expand
Oleanolic acid ameliorates cognitive dysfunction caused by cholinergic blockade via TrkB-dependent BDNF signaling
TLDR
Results imply that oleanolic acid ameliorates scopolamine‐induced memory impairment by modulating the BDNF‐ERK1/2‐CREB pathway through TrkB activation in mice, suggesting that o Leanolic acid would be a potential therapeutic agent for the treatment of cognitive deficits. Expand
The memory-enhancing effect of erucic acid on scopolamine-induced cognitive impairment in mice
TLDR
Erucic acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic acid is partially due to the activation of PI3K-PKCζ-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus. Expand
...
1
2
3
4
5
...