• Korean Journal of Pharmacognosy
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• v.39 no.2
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• pp.75-79
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• 2008

Nerve growth factor (NGF) is a protein plays a major role in the development and maintenance of central and peripheral nervous system. Recent data suggest that reduced availability of NGF may play a significant role in the pathogenesis of diabetic $polyneuropathy.^{1)}$ In our previous study, steroidal saponin from Liriope platyphylla showed neurotrophic effect by stimulation of NGF synthesis and activation of tyrosine kinase $signaling.^{2)}$ In this study, we examined the neurotrophic effect of Liriope platyphylla (LP); which was from Mylyang(MYL) and Cheongyang(CHE), and Ophiopogon japonicus (CHI) on in vitro and in vivo model for the comparison of their NGF induction. We quantitatively analyzed spicatoside A in the LP and CHI by HPLC. And we investigated the correlation between the contents of spicatoside A and NGF induction efficacy on PC 12 cells and mouse serum. These results suggest that spicatoside A may enhance NGF induction in animal model.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.21-30
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• 1998

Ginseng root has been considered to prevent neuronal degeneration associated with brain ischemia, but experimental proof in support of this speculation is limited. Moreover, few studies have compared the neuroprotective actions of ginseng ingredients with those of peptide growth factors and cytokines isf vivo. Using a gerbil forebrain ischemia model, we demonstrated that the oral administration of red ginseng powder before an ischemic insult prevents delayed neuronal death in the hippocampal CAI field and that a neuroprotective molecule within red ginseng powder is ginsenoside Rbl. The neurotrophic effect of ginsenoside Rbl, when examined in the gerbil ischemia model and in neuronal cultures was as potent as or more potent than the effects of epidermal growth factor, ciliary neurotrophic factor, erythropoietin, prosaposin, interleukin-6 and interleukin-3. Besides the protection of hippocampal CAI neurons against brain ischemia/repercussion injuries, ginsenoside Rbl was shown to prevent place navigation disability, cortical infarction and secondary thalamic degeneration in stroke-prone spontaneous hypertensive rats with permanent occlusion of the unilateral middle cerebral artery distal to the striate branches. These findings may validate the empirical use of ginseng root for the treatment of cerebrovascular diseases

• Journal of Physiology & Pathology in Korean Medicine
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• v.25 no.1
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• pp.37-47
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• 2011

This study was aimed to investigate the memory enhancing effect of Jeongjihwan against scopolamine-induced amnesia in C57BL/6 mice. To determine the effect of Jeongjihwan on the memory and cognitive function, we have injected scopolamine (1 mg/kg, i.p.) into C57BL/6 mice 30 min before beginning of behavior tests. We have conducted Y-maze, Morris water-maze, passive avoidance and fear conditioning tests to compare learning and memory functions. Scopolamine-induced behavior changes of memory impairment were significantly restored by oral administration of Jeongjihwan (100 or 200 mg/kg/day). To elucidate the molecular mechanism underlying the memory enhancing effect of Jeongjihwan, we have examined the antioxidant defense system and neurotrophic factors. Jeongjihwan treatment attenuated intracellular accumulation of reactive oxygen species and up-regulated mRNA and protein expression of antioxidant enzymes as assessed by RT-PCR and western blot analysis, respectively. Jeongjihwan also increased protein levels of brain-derived neurotrophic factor (BDNF) compared with those in the scopolamine-treated group. Furthermore, as an upstream regulator, the activation of cAMP response element-binding protein (CREB) via phosphorylation was assessed by Western blot analysis. Jeongjihwan elevated the phosphorylation of CREB (p-CREB), which seemed to be mediated partly by extracellular signal-regulated kinase1/2 (ERK1/2) and protein kinase B/Akt. These findings suggest that Jeongjihwan may have preventive and therapeutic potential in the management of amnesia.

• Journal of Life Science
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• v.26 no.1
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• pp.129-139
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• 2016

Exercise increases the expression and interaction of major neurotrophic factors such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF) at both central and peripheral tissues, which contributes to improved brain and neural plasticity and cognitive function. Previous findings have been to understand the effect of light or moderate intensity aerobic exercise on neurotrophic factors and cognitive function, not that of high intensity aerobic exercise. However, recent findings suggest that high intensity interval training is a safe, less time-consuming, efficient way to improve cardiorespiratory fitness and weight control, thus American College of Sport Medicine (ACSM)’s guidelines for exercise prescription for various adult populations also recommend the application of high intensity interval training to promote their overall health. High intensity interval training also enhances the expression of BDNF, IGF-1, and VEGF at the brain and peripheral tissues, which improves cognitive function. Increased frequency of intermittent hypoxia and increased usage of lactate as a supplementary metabolic resource at the brain and neural components are considered a putative physiological mechanism by which high intensity interval training improves neurotrophic factors and cognitive function. Therefore, future studies are required to understand how increased hypoxia and lactate usage leads to the improvement of neurotrophic factors and what the related biological mechanisms are. In addition, by comparing with the iso-caloric moderate continuous exercise, the superiority of high intensity interval training on the expression of neurotrophic factors and cognitive function should be demonstrated by associated future studies.

• Natural Product Sciences
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• v.19 no.4
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• pp.324-328
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• 2013

Soy (Glycine max, family Leguminosae) contains isoflavones and saponins as main constituents. In our preliminary study, soybean ethanol extract (SE) ameliorated scopolamine-induced memory impairment in mice in the passive avoidance task. Therefore, to confirm its ameliorating effect for memory impairments, we measured its effect in scopolamine-induced memory-impaired mice in Morris water maze task. SE significantly prevented scopolamine-induced memory impairment in the Morris water maze task. SE also increased the swimming time within quadrant section of the platform on the day after the final training session test. SE protected the reduction of brain-derived neurotrophic factor (BDNF) expression and cAMP response element-binding protein (CREB) phosphorylation in the hippocampi of scopolamine-treated mice. However, SE did not inhibit acetylcholinesterase. To understand the possible role of soysaponins in memory impairments, we prepared soyasaponins-rich (butanol) fraction of soybean (SRF) and investigated its protective effect against in the passive avoidance and Morris water maze tasks. SRF ameliorated scopolamine-induced memory impairment in mice. The memory impairment-ameliorating effect of SRF was more effective than that of SE. Based on these findings, soybean may improve memory impairment by regulating CREB phosphorylation and BDNF expression.

• The Korean Journal of Pain
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• v.31 no.3
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• pp.174-182
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• 2018

Background: The trigeminal nucleus caudalis (Vc) is a primary central site for trigeminal transmitting. Noxious stimulation of the trigeminal nociceptors alters the central synaptic releases and neural expression of some inflammatory and trophic agents. Orexin-A and the orexin 1 receptor (OX1R) are expressed in pain pathways including trigeminal pain transmission. However, the the mechanism(s) underling orexin-A effects on trigeminal pain modulation have not been fully clarified. Methods: Trigeminal pain was induced by subcutaneous injection of capsaicin in the upper lip in rats. The effect of trigeminal pain on cyclooxygenase-2 (COX-2) and brain-derived neurotrophic factor (BDNF) expression in the Vc of animals was determined by immunofluorescence. Subsequently, OX1R agonist (orexin-A) and antagonist (SB-334867-A) was administrated in the Vc to investigate the possible roles of the Vc OX1R on changes in COX-2 and BDNF levels following pain induction. Results: The data indicated an increase in COX-2 and decrease in BDNF immuno-reactivity in the Vc of capsaicin, and capsaicin- pretreated with SB-334867-A (80 nM), groups of rat. However, the effect of capsaicin on COX-2 and BDNF expressions was reversed by a Vc microinjection of orexin-A (100 pM). Conclusions: Overall, the present data reveals that orexin-A can attenuate capsaicin-induced trigeminal pain through the modulation of pain effects on COX-2 and BDNF expressions in the Vc of rats.

• 대한생식의학회:학술대회논문집
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• 2002.05a
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• pp.74.2-75
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• 2002

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.140.1-140.1
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• 2001

• Biomolecules & Therapeutics
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• v.22 no.5
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• pp.467-473
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• 2014

The purpose of this study is to investigate the memory enhancing effect and underlying molecular mechanism of arabinoxylan (AX), a major component of dietary fiber in wheat against scopolamine (SCO)-induced amnesia in Sprague-Dawley (SD) rats. Diverse behavior tests including Y-maze, Morris water maze, and passive avoidance tests were performed to measure cognitive functions. SCO significantly decreased the spontaneous alterations in Y-maze test and step-through latency in passive avoidance test, whereas increased time spent to find the hidden platform in Morris water maze test compared with the sham control group. In contrast, oral administration of AX (25 mg/kg and 50 mg/kg) effectively reversed the SCO-induced cognitive impairments in SD rats. Furthermore, AX treatment up-regulated the expression of brain-derived neurotrophic factor (BDNF) in the cortex and hippocampus via promoting activation of cAMP response element binding protein (CREB). Therefore, our findings suggest that AX can improve SCO-induced learning and memory impairment possibly through activation of CREB and up-regulation of BDNF levels, thereby exhibiting a cognition-enhancing potential.

• Journal of Magnetics
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• v.16 no.3
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• pp.253-258
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• 2011

The purpose of this study was to identify the effect of pulsed electromagnetic fields on the expression of neurotrophic factors after spinal cord injury. Sprague-Dawley male rats were given a spinal cord hemisection and randomly divided into 2 groups, the control and experimental groups. The experimental group was administered a fifteen minutes session of pulsed electromagnetic field once a day, five days a week. In order to observe the effect of these pulsed electromagnetic fields, this study observed the BDNF expression in the rat's lumbar spinal cord and the H&E staining in the gastrocnemius at 3, 7, 14, 21 days group after spinal cord hemisection. The results of this showed that the immunoreactivity of the BDNF in the rat's spinal cord gradually increased in each group. At 21 days, there is a significant difference between the control and experimental groups. The morphological shape of the gastrocnemius was gradually changed from 3days to 21days, and the gastrocnemius at 21 days was significantly degraded. However, the experimental group showed a slightly more organized gastrocnemius than the control group at 21days. The Results of this study suggest that pulsed electromagnetic field application decreases the degeneration of a rat's gastrocnemius morphology, and increases the immunoreactivity of the BDNF in the rat's spinal cord after spinal cord hemisection.