• BMB Reports
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• 제45권9호
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• pp.521-525
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• 2012

In addition to its pivotal role in neuronal survival, PI3K/Akt signaling is integral to neuronal differentiation and neurite outgrowth. However, the exact role of Akt in neuronal differentiation is still controversial. Here, we found that nuclear expression of CA-Akt resulted in unusual rapid neurite outgrowth and overexpression of KD-Akt caused multiple dendrite growth without specific axon elongation. Moreover, microarray data revealed that the expression of FOXQ1 expression was about 10-fold higher in cells with nuclear, active Akt than in control cells. Quantitative real-time PCR analysis showed that mRNA levels were upregulated in NLS-CA-Akt cells as compared to KD or EV cells. Furthermore, our FACS analysis demonstrated that overexpression of NLS-CA-Akt accumulate cells in the G1 phase within 24 h, fitting with the rapid sprouting of neuritis. Thus, our data implied that at least in this early time frame, the overexpression of nuclear, active Akt forced cells into neurite development through probably FOXQ1regulation.

• 대한임상검사과학회지
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• 제47권1호
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• pp.51-58
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• 2015

Ethanol has long been implicated in triggering apoptotic neurodegeneration. Alcohol also may indirectly harm the fetus by imparing the mother's physiology. We examined the effects of ethanol on immature brain of mice. Three-weeks-old female ICR strain mice daily intraperitoneally injected with ethanol at the concentration of 4 and 20% in saline for 0, 6, and 24 hours and 1 and 4 weeks. The mice were weighted and sacrificed, and the brains were ectomized for the present histological, immunohistochemical and TUNEL assays. Based on the histologic hematoxylin and eosin stain, immunohistochemical expression of glutamate receptor protein and neuronal cell adhesion molecule (NCAM) were evaluated. The cerebral cortex of the ethanol-treated group showed few typical symptoms of apoptosis such as chromosome condensation and disintegration of the cell bodies. TUNEL staining revealed DNA fragmentation in the 6 and 24 hours. This results demonstrated that acute ethanol administration causes neuronal cell death. I found that either glutamate receptor inhibition or activation could induce cerebellar degeneration as ethanol effect. Neuronal death also can be induced by excess activity of certain neurotransmitter, including glutamate. Neurons must establish cell-to-cell contact during growth and development in order to survive, migrate to their final destination, and develop appropriate connections with neighboring cell. Purkinje cell in cerebellar are especially vulnerable to the cell death and degeneration. After ethanol treatment in cerebellar, NCAM had decreased by 4 weeks. This result suggest that apoptosis seems to be involved in the slow elimination of neuron and cerebellar degeneration.

• Journal of Microbiology and Biotechnology
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• 제19권11호
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• pp.1490-1495
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• 2009

The development of nanotechnology has penetrated the fields of biology and medicine, resulting in remarkable applications for tissue regeneration. In order to apply this technology to tissue engineering, we have developed nano-scaled 3D scaffolds consisting of growth factor-loaded heparin/poly(l-lysine) nanoparticles (NPs) attached to the surface of polymeric micro spheres via polyionic complex methods. Growth factor-loaded NPs were simply produced as polyelectrolyte complexes with diameters of 100-200 nm. They were then coated onto positively charged poly(lactic-co-glycolic acid) (PLGA) pretreated with polyethyleneimine to enable cell adhesion, proliferation, and stimulation of neurite outgrowth. Propidium iodide staining and $\beta$-tubulin analysis revealed that neuronal PC12 cells proliferated extensively, expressed significant amounts of b-tubulin, and showed well-structured neurite outgrowth on polymeric microspheres by stimulation with growth factors. These results suggest that cellular adhesion and biological functionality on prepared PLGA microspheres enabled terminal differentiation of neuronal cells.

• 생물정신의학
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• 제30권1호
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• pp.1-6
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• 2023

Many psychiatric disorders are associated with brain functional dysfunctions and neuronal degeneration. According to the research so far, enhanced brain plasticity reduces neurodegeneration and recovers neuronal damage. Brain-derived neurotrophic factor (BDNF) is one of the most extensively studied neurotrophins in the mammalian brain that plays major roles in neuronal survival, development, growth, and maintenance of neurons in brain circuits related to emotion and cognitive function. Also, BDNF plays an important role in brain plasticity, influencing dendritic spines in the hippocampus neurogenesis. Changes in neurogenesis and dendritic density can improve psychiatric symptoms and cognitive functions. BDNF has potent effects on brain plasticity through biochemical mechanisms, cellular signal pathways, and epigenetic changes. There are pharmacological and non-pharmacological interventions to increase the expression of BDNF and enhance brain plasticity. Non-pharmacological interventions such as physical exercise, nutritional change, environmental enrichment, and neuromodulation have biological mechanisms that increase the expression of BDNF and brain plasticity. Non-pharmacological interventions are cost-effective and safe ways to improve psychiatric symptoms.

• Natural Product Sciences
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• 제15권4호
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• pp.198-202
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• 2009

Based on the use of Acorus gramineus SOLAND (AG) for the treatment of stroke in traditional Korean medicine, the present study was carried out to evaluate neuroprotective effects of ${\alpha}$-asarone after transient global cerebral ischemia using rat 4-vessel occlusion (4VO) model in rats. ${\alpha}$-Asarone (5 mg/kg) administered intraperitoneally significantly protected CA1 neurons against 10 min transient forebrain ischemia as demonstrated by measuring the density of neuronal cells stained with Cresyl violet. ${\alpha}$-Asarone significantly reduced hippocampal neuronal cell death by 85.2% where as its isolated single compounds from AG compared with a vehicle-treated group.

• Molecules and Cells
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• 제38권1호
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• pp.51-57
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• 2015

The Caenorhabditis elegans peroxidasins, PXN-1 and PXN-2, are extracellular peroxidases; pxn-2 is involved in muscle-epidermal attachment during embryonic morphogenesis and in specific axon guidance. Here we investigate potential roles of the other homologue of peroxidasin, pxn-1, in C. elegans. A pxn-1 deletion mutant showed high lethality under heat-stress conditions. Using a transcriptional GFP reporter, pxn-1 expression was observed in various tissues including neurons, muscles, and hypodermis. A translational fusion showed that PXN-1::GFP was secreted and localized in extracellular matrix, particularly along body wall muscles and pharyngeal muscles. Various neuronal developmental defects were observed in pxn-1 mutants and in pxn-1 over-expressing animals, including handedness, branching, breakage, tangling, and defasciculation. These results suggest that pxn-1, like other peroxidasins, plays an important role throughout development.

• Molecules and Cells
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• 제27권5호
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• pp.609-613
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• 2009

It has been reported that selenoprotein W (SelW) mRNA is highly expressed in the developing central nerve system of rats, and its expression is maintained until the early postnatal stage. We here found that SelW protein significantly increased in mouse brains of postnatal day 8 and 20 relative to embryonic day 15. This was accompanied by increased expression of SOD1 and SOD2. When the expression of SelW in primary cultured cells derived from embryonic cerebral cortex was knocked down with small interfering RNAs (siRNAs), SelW siRNA-transfected neuronal cells were more sensitive to the oxidative stress induced by treatment of $H_2O_2$ than control cells. TUNEL assays revealed that $H_2O_2$-induced apoptotic cell death occurred at a higher frequency in the siRNA-transfected cells than in the control cells. Taken together, our findings suggest that SelW plays an important role in protection of neurons from oxidative stress during neuronal development.

• Journal of Ginseng Research
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• 제42권4호
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• pp.429-435
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• 2018

Background: Recent studies have shown that Korean Red Ginseng (KRG) successfully protects against dopaminergic neuronal death in the nigrostriatal pathway of a Parkinson's disease (PD) mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration; however, the mechanism has yet to be identified. Therefore, in this study we used two-dimensional electrophoresis to investigate the effects of KRG on the changes in protein expression in the substantia nigra (SN) of MPTP-treated mice. Methods: Male C57BL/6 mice (9 wk old) were intraperitoneally administered MPTP (20 mg/kg) four times at 2-h intervals, after which KRG (100 mg/kg) was orally administered once a day for 5 d. Two hours after the fifth KRG administration, a pole test was conducted to evaluate motor function, after which the brains were immediately collected. Survival of dopaminergic neurons was measured by immunohistochemistry, and protein expression was measured by two-dimensional electrophoresis and Western blotting. Results: KRG alleviated MPTP-induced behavioral dysfunction and neuronal toxicity in the SN. Additionally, the expression of eight proteins related to neuronal formation and energy metabolism for survival were shown to have changed significantly in response to MPTP treatment or KRG administration. KRG alleviated the downregulated protein expression following MPTP administration, indicating that it may enhance neuronal development and survival in the SN of MPTP-treated mice. Conclusion: These findings indicate that KRG may have therapeutic potential for the treatment of patients with PD.

• Journal of Nutrition and Health
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• 제32권8호
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• pp.864-869
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• 1999

To investigate the effect of dietary phosphatidylcholine(PPC) supplement on memory improvement, biochemical study on the brain, and morphometric studies on the cholinergic neurons in the rat basal forebrain were undertaken. The pregnancy rats were divided into the normal control, the choline deficient and the PPC supplemental groups according to quantity of the PPC in diet. According to choline deficiency and PPC supplement after birth, the neonate rate of the normal control group were subdivided into the control diet(N-N) and the PPC supplied (N-S) groups, the choline deficient group were subdivided into the continually deficient (D-D), the control diet(D-N) and the PPC supplied groups(D-S), and the PPC supplemental group were subdivided into the control diet (S-N)and the continually supplied (S-S)group. The PPC supplemented diet was added 2% egg PPC in AIN 76 formula diet. PPC concentrations and cholinesterase(CE) activities were measured in the serum, the liver and the brain, respectively. Immunohistochemical stains for choline acetyltransferase(ChAT) was employed for the morphological and morphometric studies. The maze test was undertaken to evaluate memory improvement. PPC concentration and CE activities in the serum, liver and the brain were high in the PPC supplemental groups and low in the choline deficient groups. ChAT immunoreactivity neurons at the medial septal diagonal bond complex and the basal forebrain nucleus of Meynert were reduced in the choline deficient groups. Average failure rate for the maze test was the lowest in the S-S group and the highest in the D-D group. Insufficient choline suppley during the neuronal development would result in cholinergic neuronal damage, which could be prevented by adequate PPC supplement. It is consequently suggested that PPC supplement may be effective on memory improvement by maintaining the cholinergic neuronal activity in the basal forebrain of the rats.

• 생명과학회지
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• 제15권3호
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• pp.505-512
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• 2005

신경흥분독성과 간질발작발현은 glutamate 수용체활성과 연관이 있다고 알려져 있다. a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA), kainate 수용체에 대한 glutamate 활성을 포함하는 다양한 기전을 가진 항전간제인 Topiramate는 신경보호작용을 가진다는 증거가 제시되어 Topiramate가 간질발작 후 해마의 glutamate 수용체 발현에 미치는 효과를 관찰하였다. 흰쥐에 kainate를 복강 내 주사하여 간질중첩증을 유발시킨 후 Topiramate를 1주일 주사하였다 Apop tag in situ detection kit를 이용하여 세포손상을 관찰한 결과 kainate 유발 간질중첩증 1주일 후 해마의 CA1, CA3에서 심각한 세포사를 보였으나, Topiramte 처리 군에서는 세포사가 현저히 감소하였다. 간질중첩증 이후 NMDA 수용체 아형 1,2a, 2b 발현이 현저히 증가했으나 Topiramate 처치에 의해 NMDA수용체의 발현에는 뚜렷한 변화가 없었다. AMPA수용체에서는 GluR1이 간질중첩증 이후 현저히 상향 조정되었고 GluR2는 현저히 하향조정 되었다 Topiramate 1주일 처리 시 간질중첩증으로 인해 변화된 CluR1과 GluR2의 발현이 역전되었다. 결론적으로 Topiramate는 간질중침증에 의한 CluR1/CluR2 발현비의 증가로 유발되는 흥분성 신경세포사를 억제시킴으로써 신경보호작용이 있는 것으로 보인다.