• The Korean Journal of Physiology and Pharmacology
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• 제26권6호
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• pp.415-425
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• 2022

Memory formation in the hippocampus is formed and maintained by circadian clock genes during sleep. Sleep deprivation (SD) can lead to memory impairment and neuroinflammation, and there remains no effective pharmacological treatment for these effects. Myricetin (MYR) is a common natural flavonoid that has various pharmacological activities. In this study, we investigated the effects of MYR on memory impairment, neuroinflammation, and neurotrophic factors in sleep-deprived rats. We analyzed SD-induced cognitive and spatial memory, as well as pro-inflammatory cytokine levels during SD. SD model rats were intraperitoneally injected with 10 and 20 mg/kg/day MYR for 14 days. MYR administration significantly ameliorated SD-induced cognitive and spatial memory deficits; it also attenuated the SD-induced inflammatory response associated with nuclear factor kappa B activation in the hippocampus. In addition, MYR enhanced the mRNA expression of brain-derived neurotropic factor (BDNF) in the hippocampus. Our results showed that MYR improved memory impairment by means of anti-inflammatory activity and appropriate regulation of BDNF expression. Our findings suggest that MYR is a potential functional ingredient that protects cognitive function from SD.

• The Journal of Korean Physical Therapy
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• 제13권2호
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• pp.281-292
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• 2001

This study was performed to investigate the effect of therapeutic exercise on brain-derived neurotrophic factor manifestation after global brain ischemia in rats. Nine rats with global ischemia were divided at random into two group. In the control group, three rats remained in cage. But, in the end, two rats were alive. In the therapeutic exercise group, six rats remained. The five rats of this group was swam for 30 minutes everyday for a week. The brain-derived neurotrophic factor expression was identified from immunohistochemistry. The results of this study were as follows : 1. In the control group, a little expression of brain-derived neurotrophic factor was observed at cortex and hippocampus layer, but cell body and axon was observed obscurely. 2. In the experimental group, a much expression of brain-derived neurotrophic factor was observed at cortex and hippocampus layer, and cell body and axon was observed clearly. In the neurological examination(beam-walking test). experimental group was obtained higher 1.4 points than control group. BDNF expression was increased by swimming for 30 minutes everyday for a week. Therefore, therapeutic exercise contribute to brain plasticity after brain ischemia.

• ALGAE
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• 제31권2호
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• pp.175-187
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• 2016

This study evaluated the effects of γ-aminobutyric acid (GABA)-enriched fermented sea tangle (GFST), as a functional food, on brain derived neurotrophic factor (BDNF)-related muscle growth and lipolysis, in a sarcopenic obesity high-risk group. Twenty-one middle-aged women (53-63 y) participated in this randomized, double-blind, placebo controlled study. Participants ingested either 1,000 mg of GFST (n = 10) or a sucrose placebo (CON) (n = 11) everyday, for 8 weeks. Subjects were asked to abstain from any regular exercise. Fasting venous blood samples, body composition and muscular strength were measured before and after supplementation period. Collectively, we demonstrated that GFST significantly decreased total fat mass and triglyceride in body composition, as well as significantly increasing serum BDNF (p < 0.001), angiotensin converting enzyme (p < 0.001), human growth hormone and insulin-like growth factor-1 levels (p < 0.05 and p < 0.05, respectively) accompanied by increased total lean mass (p < 0.01). Furthermore, the reported improvements in total work, knee extension and flexion at 60° s⁻¹ (p < 0.05), and peak torque normalized to body weight of knee flexion at 60° s⁻¹ (p < 0.05), support an ergogenic effect of GABA associated with increased growth factor levels. The use of GFST, as a functional food ingredient, to elicit anti-obesity effects and stimulate the release of muscle-related growth factors with increasing serum BDNF levels may provide a protective intervention for age-related degeneration such as sarcopenic obesity.

• 대한한의학회지
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• 제30권3호
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• pp.39-50
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• 2009

Objective : The aim of this study was to evaluate the effects of Aconiti ciliare tuber on the descending pain and the recovery of locomotor function that results from sciatic crushed nerve injury in rats. Method : In order to assess the effects of the aqueous extract of Aconiti ciliare tuber on the recovery rate of locomotor function, we investigated the walking track analysis, and for the effects on the pain control we investigated brain-derived neurotrophic factor (BDNF) and inducible nitric oxide synthase (iNOS) expression in the sciatic nerve and on the expressions of c-Fos in the ventrolateral periaqueductal gray (vlPAG) region resulting from the sciatic crushed nerve injury in rats. Result : Treatment with Aconiti ciliare tuber significantly enhanced the SFIvalue, enhanced BDNF expression, decreased iNOS expression, and suppressed c-Fos expression. The present results showed that Aconiti ciliare tuber facilitated functional recovery following sciatic crushed nerve injury in rats. The recovery mechanisms of SFI by Aconiti ciliare tuber might be ascribed to the increase of BDNF expression for nerve regeneration and reinnervation and to the suppression of iNOS expression for inhibiting nerve inflammation. Conclusion : In this process it has been shown that Aconiti ciliare tuber can be used for pain control and functional recovery from peripheral nerve injury.

• 한국어업기술학회:학술대회논문집
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• 한국어업기술학회 2002년도 춘계 수산관련학회 공둥학술발표회
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• pp.177-178
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• 2002

• 생명과학회지
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• 제17권11호
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• pp.1464-1471
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• 2007

당뇨병은 만성적 대사질환으로 말초뿐만 아니라 중추신경계에서도 다양한 합병증을 유발시키는 것으로 알려져 있다. 특히, 당뇨환자는 인지기능의 손상으로 인해 치매 유병율이 높은 것으로 보고되고 있다. 규칙적인 운동은 당뇨병의 이차 합병증을 예방하기 위한 치료적 방법으로 흔히 권장된다. 이에 본 연구는 당뇨흰쥐를 대상으로 트레드밀 운동이 기억력과 해마 BDNF 발현에 미치는 효과를 조사하였다. SD계열 흰쥐를 실험동물로 하여 STZ (50 mg/kg) 투여로 유발시킨 당뇨흰쥐를 8주간 주 5회 30분씩 트레드밀에서 달리도록 하였다. 운동프로그램 종료 후, Morris water maze로 기억력을 측정하고, 해마조직을 적출하여 Western으로 brain-derived neurotrophic factor (BDNF) 발현을 정량화하였다. 본 연구결과 8주간의 당뇨는 선행연구과 유사하게 기억력 손상과 함께 해마 조직의 BDNF 발현을 유의하게 감소시키는 것으로 나타났다. 하지만 트레드밀 운동은 당뇨흰쥐에서 기억력과 해마 BDNF 발현을 유의하게 향상시키는 것으로 나타났다. 이러한 결과는 당뇨동물에서 운동이 해마 BDNF 발현의 증가를 통해 인지기능의 손상을 완화시킬 수 있음을 보여주는 것이다.

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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• pp.18-18
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• 2002

This study was to investigate the effect of neurotrophic factors on neural cell differentiation in vitro derived from human embryonic stem (hES, MB03) cells. For neural progenitor cell formation derived from hES cells, we produced embryoid bodies (EB: for 5 days, without mitogen) from hES cells and then neurospheres (for 7 - 10 days, 20 ng/㎖ of bFGF added N2 medium) from EB. And then finally for the differentiation into mature neuron cells, neural progenitor cells were cultured in ⅰ) N2 medium (without bFGF), ⅱ) N2 supplemented with brain derived neurotrophic factor (BDNF, 5ng/㎖) or ⅲ) N2 supplemented with platelet derived growth factor-bb (PDGF-bb, 20ng/㎖) for 2 weeks. (omitted)

• 생명과학회지
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• 제27권8호
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• pp.879-887
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• 2017

히스톤 탈 아세틸 효소(HDAC)와 인슐린유사성장인자(IGF-I)는 근육 관련 유전자들의 활성 및 발현을 조절하여 골격근의 성장 및 발달을 조절하지만 이들이 근신경계 발달 및 대사 기능에 중요한 역할을 담당하는 뇌신경성장인자(BDNF)의 발현에 미치는 영향에 관한 연구는 거의 이루어지지 않았다. 따라서 본 연구에서는 IGF-I과 HDAC의 억제제인 SAHA가 C2C12 골격근 세포에서 BDNF 발현에 미치는 영향을 알아보고자 하였다. 그 결과 IGF-I은 농도와 시간 의존적으로 BDNF의 mRNA 및 단백질 발현을 감소시켰지만 HDAC을 억제하자 IGF-I에 의해 감소되었던 BDNF의 발현이 증가하는 경향을 관찰할 수 있었다. 따라서 IGF-I은 BDNF의 발현을 억제하며, HDAC의 억제는 IGF-I에 의한 BDNF의 발현 억제를 감소시킬 수 있다는 사실을 확인할 수 있었다.

• 생물정신의학
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• 제12권2호
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• pp.189-195
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• 2005

Objects:Some studies have suggested that brain-derived neurotrophic factor(BDNF), one of the most important neurotrophins, is involved in pathophysiology of depression and suicide. This study was performed to determine whether there is an abnormality in plasma BDNF concentration in suicidal attempters. Methods:The subjects were 71 suicidal attempters who visited emergency rooms in multi-medical centers. All subjects had been interviewed by using Structured Clinical Interview for DSM-IV(SCID), Hamilton Depression Rating Scale(HDRS), Young Mania Rating Scale(YMRS), and Positive And Negative Syndrome Scale(PANSS). The severity of the suicidal behavior was measured by Lethality of Suicide Attempt Rating Scale(LSARS) and Risk-Rescue Rating(RRR) system. Seventy-one age, sex, and diagnosis matched non-suicidal psychiatric patients who were consecutively admitted to a psychiatric ward during the same period recruited as psychiatric controls. They were drug-naive or drug-free at least more than 2 months. In addition, 80 healthy controls were randomly selected as normal controls. Plasma BDNF level was measured by the enzyme linked immunosorbent assay(ELISA) methods. Results:In overall F-test, differences of the plasma BDNF levels among the groups were statistically significant(F=20.226, p<0.001). In the multiple comparisons(Scheffe), while mean levels of plasma BDNF between normal controls and non-suicidal psychiatric patients were similar(p=0.984), the BDNF levels of suicidal attempters were lower than those of other two groups(p<0.001). LSARS and RRR did not reveal any significant correlations with BDNF levels in suicidal attempters. Conclusion:These results suggest that reduction of plasma BDNF level is related to suicidal behavior and BDNF level may be a biological marker of suicidal behavior.

• The Korean Journal of Pain
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• 제36권1호
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• pp.72-83
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• 2023

Background: Globally, spinal cord injury (SCI) results in a big burden, including 90% suffering permanent disability, and 60%-69% experiencing neuropathic pain. The main causes are oxidative stress, inflammation, and degeneration. The efficacy of the stem cell secretome is promising, but the role of human neural stem cell (HNSC)-secretome in neuropathic pain is unclear. This study evaluated how the mechanism of HNSC-secretome improves neuropathic pain and locomotor function in SCI rat models through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities. Methods: A proper experimental study investigated 15 Rattus norvegicus divided into normal, control, and treatment groups (30 µL HNSC-secretome, intrathecal in the level of T10, three days post-traumatic SCI). Twenty-eight days post-injury, specimens were collected, and matrix metalloproteinase (MMP)-9, F2-Isoprostanes, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, and brain derived neurotrophic factor (BDNF) were analyzed. Locomotor recovery was evaluated via Basso, Beattie, and Bresnahan scores. Neuropathic pain was evaluated using the Rat Grimace Scale. Results: The HNSC-secretome could improve locomotor recovery and neuropathic pain, decrease F2-Isoprostane (antioxidant), decrease MMP-9 and TNF-α (anti-inflammatory), as well as modulate TGF-β and BDNF (neurotrophic factor). Moreover, HNSC-secretomes maintain the extracellular matrix of SCI by reducing the matrix degradation effect of MMP-9 and increasing the collagen formation effect of TGF-β as a resistor of glial scar formation. Conclusions: The present study demonstrated the mechanism of HNSC-secretome in improving neuropathic pain and locomotor function in SCI through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities.