• Journal of Integrative Natural Science
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• v.8 no.2
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• pp.81-88
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• 2015

c-Jun N-terminal kinase-3 (JNK3) is a member of the mitogen-activated protein kinase family (MAPK), and plays an important role in neurological disorders. Therefore, identification of selective JNK3 inhibitor may contribute towards neuroprotection therapies. In this work, we performed hologram quantitative structure-activity relationship (HQSAR) on a series of thiophene trisubstituted derivatives. The best predictions were obtained for HQSAR model with $q^2=0.628$ and $r^2=0.986$. Statistical parameters from the generated QSAR models indicated the data is well fitted and have high predictive ability. HQSAR result showed that atom, bond and chirality descriptors play an important role in JNK3 activity and also shows that electronegative groups is highly favourble to enhance the biological activity. Our results could be useful to design novel and selective JNK3 inhibitors.

• Advances in Traditional Medicine
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• v.7 no.5
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• pp.564-568
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• 2008

The root of Polygala tenuifolia Willd (PT) is known to have neuroprotective effects and as an antidementic herb in Chinese and Japanese traditional medicine. We examined potential neuroprotective effects of PT using the 4-vessel occlusion model in rats. In this study, the efficacy of PT for the prevention of neuronal damage and for the reduction of memory impairment was investigated. The results indicate that PT confers significant neuroprotection especially for ischemic hippocampal neurons.

• Clinical and Experimental Pediatrics
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• v.58 no.7
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• pp.239-244
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• 2015

The complement system is part of the innate immune response and as such defends against invading pathogens, removes immune complexes and damaged self-cells, aids organ regeneration, confers neuroprotection, and engages with the adaptive immune response via T and B cells. Complement activation can either benefit or harm the host organism; thus, the complement system must maintain a balance between activation on foreign or modified self surfaces and inhibition on intact host cells. Complement regulators are essential for maintaining this balance and are classified as soluble regulators, such as factor H, and membrane-bound regulators. Defective complement regulators can damage the host cell and result in the accumulation of immunological debris. Moreover, defective regulators are associated with several autoimmune diseases such as atypical hemolytic uremic syndrome, dense deposit disease, age-related macular degeneration, and systemic lupus erythematosus. Therefore, understanding the molecular mechanisms by which the complement system is regulated is important for the development of novel therapies for complement-associated diseases.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.115-120
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• 2018

Chronic cerebral hypoperfusion (CCH), which is associated with onset of vascular dementia, causes cognitive impairment and neuropathological alterations in the brain. In the present study, we examined the neuroprotective effect of duloxetine (DXT), a potent and balanced serotonin/norepinephrine reuptake inhibitor, on CCH-induced neuronal damage in the hippocampal CA1 region using a rat model of permanent bilateral common carotid arteries occlusion. We found that treatment with 20 mg/kg DXT could attenuate the neuronal damage, the reduction of phosphorylations of mTOR and p70S6K as well as the elevations of $TNF-{\alpha}$ and $IL-1{\beta}$ levels in the hippocampal CA1 region at 28 days following CCH. These results indicate that DXT displays the neuroprotective effect against CCH-induced hippocampal neuronal death, and that neuroprotective effect of DXT may be closely related with the attenuations of CCH-induced decrease of mTOR/p70S6K signaling pathway as well as CCH-induced neuroinflammatory process.

• Food Science and Biotechnology
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• v.16 no.4
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• pp.632-635
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• 2007

This study examined the neuroprotective effect of scopoletin from Angelica dahurica against oxygen and glucose deprivation-induced neurotoxicity in a rat organotypic hippocampal slice culture. Scopoletin reduced the propidium iodide (PI) uptake, which is an indication of impaired cell membrane integrity. In addition, it inhibited the loss of NeuN, which represents the viability of neuronal cells. The results suggests that scopoletin from A. dahurica protects neuronal cells from the damage caused by oxygen and glucose deprivation.

• Journal of Ginseng Research
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• v.36 no.4
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• pp.342-353
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• 2012

Ginseng, the root of the Panax ginseng, has been a popular and widely-used traditional herbal medicine in Korea, China, and Japan for thousands of years. Now it has become popular as a functional health food and is used globally as a natural medicine. Evidence is accumulating in the literature on the physiological and pharmacological effects of P. ginseng on neurodegenerative diseases. Possible ginseng- or ginsenosides-mediated neuroprotective mechanisms mainly involve maintaining homeostasis, and anti-inflammatory, anti-oxidant, anti-apoptotic, and immune-stimulatory activities. This review considers publications dealing with the various actions of P. ginseng that are indicative of possible neurotherapeutic efficacies in neurodegenerative diseases and neurological disorders such as Parkinson's disease, Alzheimer's disease, Huntington's disease, and amyotrophic lateral sclerosis and multiple sclerosis.

• Archives of Pharmacal Research
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• v.29 no.11
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• pp.963-968
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• 2006

Seven phenolic compounds (1-7) were isolated from the tubers of Gastrodia elata. Their structures were elucidated on the basis of MS and NMR spectral data. p-Ethoxymethyl phenyl-O-${\beta}$-D-glucoside (1) was proved to be a new compound, with N-(p-hydroxybenzyl)-adenosine (7) isolated from this plant for the first time. In this study, the protective effects of the six constituents (1-6) on PC12 cells against the cytotoxicity induced by KCI and glutamate were also investigated. The viability of the PC12 cells was significantly enhanced by pretreatment with the six phenolic constituents.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.223-229
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• 2006

The emerging concept of the 'neurovascular unit' may enable a powerful paradigm shift for neuroscience. Instead of a pure focus on the 'neurobiology' of disease, an opportunity now exists to return to a more integrative approach. The neurovascular unit emphasizes that signaling between vascular and neuronal compartments comprise the basis for both function and dysfunction in brain. Hence, brain disorders are not just due to death of neurons, but instead manifested as cell signaling perturbations at the neurovascular interface. In this mini-review, we will examine 3 examples of this hypothesis: neurovascular mechanisms involved in the thrombolytic therapy of stroke, the crosstalk between neurogenesis and angiogenesis, and the link between vascular dysfunction and amyloid pathology in Alzheimer's disease. An understanding of cell-cell and cell-matrix signaling at the neurovascular interface may yield new approaches for targeting CNS disorders.

• Fisheries and Aquatic Sciences
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• v.22 no.5
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• pp.10.1-10.14
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• 2019

Fish skin waste accounts for part of the solid waste generated from seafood processing. Utilization of fish skin by bioconversion into high-grade products would potentially reduce pollution and economic cost associated with treating fish processing waste. Fish skin is an abundant supply of gelatin and collagen which can be hydrolyzed to produce bioactive peptides of 2-20 amino acid sequences. Bioactivity of peptides purified from fish skin includes a range of activities such as antihypertensive, anti-oxidative, antimicrobial, neuroprotection, antihyperglycemic, and anti-aging. Fish skin acts as a physical barrier and chemical barrier through antimicrobial peptide innate immune action and other functional peptides. Small peptides have been demonstrated to possess biological activities which are based on their amino acid composition and sequence. Fish skin-derived peptides contain a high content of hydrophobic amino acids which contribute to the antioxidant and angiotensin-converting enzyme inhibitory activity. The peptide-specific composition and sequence discussed in this review can be potentially utilized in the development of pharmaceutical and nutraceutical products.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.45 no.5
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• pp.233-240
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• 2019

Trigeminal nerve injury as a consequence of lower third molar surgery is a notorious complication and may affect the patient in long term. Inferior alveolar nerve (IAN) and lingual nerve (LN) injury result in different degree of neurosensory deficit and also other neurological symptoms. The long term effects may include persistent sensory loss, chronic pain and depression. It is crucial to understand the pathophysiology of the nerve injury from lower third molar surgery. Surgery remains the most promising treatment in moderate-to-severe nerve injuries. There are limitations in the current treatment methods and full recovery is not commonly achievable. It is better to prevent nerve injury than to treat with unpredictable results. Coronectomy has been proved to be effective in reducing IAN injury and carries minimal long-term morbidity. New technologies, like the roles of erythropoietin and stem cell therapy, are being investigated for neuroprotection and neural regeneration. Breakthroughs in basic and translational research are required to improve the clinical outcomes of the current treatment modalities of third molar surgery-related nerve injury.