• Proceedings of the Korean Society of Applied Pharmacology
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• 2000.04a
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• pp.15-16
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• 2000

Transient forebrain ischemia results in delayed neuronal death in the CA1 region of the hippocampus after injury, which is, at least in part, a consequence of excessive generation of reactive oxygen species. Previous in vitro studies using cell cultures or brain slices have demonstrated that phospholipase D (PLD) in the nervous system is involved in the signaling mechanism in response to a variety of agonists. Several recent studies have shown that reactive oxygen species stimulate phospholipase D (PLD) activity in several kinds of cells. Therefore, this raises the possibility that PLD activity is enhanced in the ischemic brain. Meanwhile, osteopontin (OPN) was initially identified as a sialoglycoprotein in bone, but has since been found in various tissues. Although not much is known about its function, OPN seems to play an important role in inflammation and tissue repair. Recently, it was reported that OPN was upregulated in the activated microglia after focal brain ischemia, suggesting that OPN might play a role in wound healing after a focal stroke.

• Korean Journal of Biological Psychiatry
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• v.18 no.4
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• pp.169-175
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• 2011

Stress, a risk factor of major depression induces cytokine mediated inflammation and decreased neurogenesis. In patients with major depression, significant increases of pro-inflammatory cytokines have been consistently reported. The pro-inflammatory cytokines can stimulate the hypothalamic-pituitary-adrenal (HPA) axis to release glucocorticoids. In the brain, microglia and play a role of immune activation in response to stress. Increased pro-inflammatory cytokine play a role in restricting neurogenesis in the brain. Although neurogenesis may not be essential for the development of depression, it may be required for clinically effective antidepressant treatment. Hence, stimulation of neurogenesis is regarded as a promising strategy for new antidepressant targets. This review introduces changes in neurotransmitter, cytokine and neurogenesis in major depression and explores the possible relationship between pro-inflammatory cytokines and neurogenesis related to stress in major depression.

• BMB Reports
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• v.41 no.5
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• pp.345-352
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• 2008

The cerebral microvessels possess barrier characteristics which are tightly sealed excluding many toxic substances and protecting neural tissues. The specialized blood-neural barriers as well as the cerebral microvascular barrier are recognized in the retina, inner ear, spinal cord, and cerebrospinal fluid. Microvascular endothelial cells in the brain closely interact with other components such as astrocytes, pericytes, perivascular microglia and neurons to form functional 'neurovascular unit'. Communication between endothelial cells and other surrounding cells enhances the barrier functions, consequently resulting in maintenance and elaboration of proper brain homeostasis. Furthermore, the disruption of the neurovascular unit is closely involved in cerebrovascular disorders. In this review, we focus on the location and function of these various blood-neural barriers, and the importance of the cell-to-cell communication for development and maintenance of the barrier integrity at the neurovascular unit. We also demonstrate the close relation between the alteration of the blood-neural barriers and cerebrovascular disorders.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.93-100
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• 2018

Carbon monoxide (CO) is a gaseous molecule produced from heme by heme oxygenase (HO). Endogenous CO production occurring at low concentrations is thought to have several useful biological roles. In mammals, especially humans, a proper neurovascular unit comprising endothelial cells, pericytes, astrocytes, microglia, and neurons is essential for the homeostasis and survival of the central nervous system (CNS). In addition, the regeneration of neurovascular systems from neural stem cells and endothelial precursor cells after CNS diseases is responsible for functional repair. This review focused on the possible role of CO/HO in the neurovascular unit in terms of neurogenesis, angiogenesis, and synaptic plasticity, ultimately leading to behavioral changes in CNS diseases. CO/HO may also enhance cellular networks among endothelial cells, pericytes, astrocytes, and neural stem cells. This review highlights the therapeutic effects of CO/HO on CNS diseases involved in neurogenesis, synaptic plasticity, and angiogenesis. Moreover, the cellular mechanisms and interactions by which CO/HO are exploited for disease prevention and their therapeutic applications in traumatic brain injury, Alzheimer's disease, and stroke are also discussed.

• Archives of Pharmacal Research
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• v.29 no.6
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• pp.469-475
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• 2006

A series of yakuchinone B 1f and its analogs 1a-e was synthesized and evaluated for free radical scavenging, suppression of LPS-induced NO generation, cytotoxicity and anti-excitotoxicity in vitro. Compound 1c exhibited potent anti-excitotoxicity, while all compounds 1a-f showed considerable effects of free radical scavenging, suppression of LPS-induced NO generation, and cytotoxicity in microglia.

• Toxicological Research
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• v.9 no.2
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• pp.233-240
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• 1993

Toxic effects of chronic adminstration of methamphetamine (MA) to SD rats were studied in respect to histopathological changes induced in each organ. In experimental groups liver weight decreased and brain weights increased markedly compared with controls in the 12th month after subcutaneous injection of 0.5 mg and 5mg/kg/BW MA. Serum alkaline phosphotase levels increased, but marked decrease of cholesterol, triglyceride, and BUN levels were checked depending on both the dose of MA and duration of treatment.

• Biomolecules & Therapeutics
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• v.19 no.4
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• pp.425-430
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• 2011

In this study, we found that Forsythiae fructus (FF) and one of its main compounds, arctigenin, significantly inhibited nitric oxide production in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Arctigenin also suppressed the expression of inducible nitric oxide synthase and cyclooxygenase-2, and inhibited the activation of extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38. Moreover, it also reduced levels of proinflammatory cytokines, interleukin $1{\beta}$, tumor necrosis factor ${\alpha}$ and prostaglandin E2, and inhibited neuronal death in LPS-treated organotypic hippocampal cultures. Therefore, we suggest that arctigenin may confer a neuroprotective effect via the inhibition of neuroinflammation.

• Biomedical Science Letters
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• v.24 no.4
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• pp.398-404
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• 2018

To evaluate the antioxidant and anti-neuroinflammatory effects of defatted Perilla frutescens extract (DPE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells. Cell viabilities were estimated by MTT assay. LPS-stimulated BV-2 microglia were used to study the expression and production of inflammatory mediators such as nitric oxide (NO), inducible NO synthase (iNOS), Cyclooxygenase-2 (COX-2), and prostaglandin $E_2$ ($PGE_2$). Pretreatment with DPE prior to LPS treatment significantly inhibited excessive production of NO (10, 25, 50, 75, and $100{\mu}g/mL$) in a dose-dependent manner, and was associated with down regulation of expression of iNOS and COX-2. DPE also suppressed the LPS-induced increase in $PGE_2$ level (10, 25, 50, 75, and $100{\mu}g/mL$) in BV-2 cells. Therefore, DPE can be considered as a useful therapeutic and preventive approach for the treatment of several neurodegenerative diseases.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.204.1-204.1
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• 2003

Azheimer's Disease (AD) known as senile dementia accounts for 50％ of all dementia cases and is in growing status as population goes up. Generally. AD is a progressive neurodegenerative disease and includes much of senile plaque in cerebral hippocampus and cortex in patient's brain. For decades. AD theory is explained by amyloid cascade hypothesis. In process of the hypothesis, amyloid hypothesis forms fibrillar form beta-amyloid peptide (A${\beta}$ peptide) and extraordinarily accumulates in brain tissue, and lastly senile plaque is formed, which pathologically affect the brain. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.208.1-208.1
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• 2003

In recent, growing aged people in coupled with the increased senile dementia, Alzheimer's disease, has been a social interests to be cleared out. Alzheimer Disease(AD), first reported by Alios Alzheimer (1864-1915) in 1907, is a neurodegenrative disease. Nothing exact cause of AD is available by now, but in clinical founding ${\beta}$-amyloid peptide(A${\beta}$) and microtubule associated protein($\tau$ protein) is to involved in the disease, and the most important feature in AD is Known to induce chronic inflammation to neuron cell. (omitted)