• Environmental Analysis Health and Toxicology
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• v.18 no.4
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• pp.249-254
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• 2003

본 연구는 환경호르몬(endocrine disruptors)으로 분류되었으며, 에스트로젠 화합물의 특성을 지닌 4-Nonylphenol (NP)이 설치류 Pituitary 세포 중 성장호르몬을 분비하는 GH3 세포의 Nitric oxide(NO)을 증가시키는 작용기전을 규명코자 수행되었다 먼저 GH3세포에 NP처리 농도에 따른 NO의 생성을 측정한 결과 NP처리농도 의존적으로 증가시켰다. 이러한 NO의 증가가 genomic action인지를 확인하기 위해 GH3세포의 NO를 증가시키는 효소인 neuronal oxide synthase의 단백질량을 측정한 결과 GH3세포에서 NP에 의한 nNOS의 단백질의 변화는 없었다. 에스트로젠 화합물인 NP가 에스트로젠 리셉터 (ER)와의 관계를 조사하기 위해 ER억제제(ICI 168,780)클 처리한 경우 NP에 의해 증가한 NO가 감소하였다. 또한 유전자 전사억제제인 actinomycin D 및 단백질 발현 억제제인 cycloheximide을 처리한 경우는 NP에 의한 NO 증가억제효과가 없었다. 이러한 결과를 종합해 볼 때 GH3 세포에서 NP는 ER을 매개한 non-genomic action에 의해 NO를 증가키는 것으로 사료된다.

• Journal of Ginseng Research
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• v.42 no.3
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• pp.239-247
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• 2018

In recent years, several therapeutic drugs have been rationally designed and synthesized based on the novel knowledge gained from investigating the actions of biologically active chemicals derived from foods, plants, and medicinal herbs. One of the major advantages of these naturalistic chemicals is their ability to interact with multiple targets in the body resulting in a combined beneficial effect. Ginseng is a perennial herb (Araliaceae family), a species within the genus Panax, and a highly valued and popular medicinal plant. Evidence for the medicinal and health benefits of Panax ginseng and its components in preventing neurodegeneration has increased significantly in the past decade. The beneficial effects of P. ginseng on neurodegenerative diseases have been attributed primarily to the antioxidative and immunomodulatory activities of its ginsenoside components. Mechanistic studies on the neuroprotective effects of ginsenosides revealed that they act not only as antioxidants but also as modulators of intracellular neuronal signaling and metabolism, cell survival/death genes, and mitochondrial function. The goal of the present paper is to provide a brief review of recent knowledge and developments concerning the beneficial effects as well as the mechanism of action of P. ginseng and its components in the treatment and prevention of neurodegenerative diseases.

• Korean Journal of Veterinary Service
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• v.27 no.4
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• pp.335-343
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• 2004

Although human rabies deaths are rare, the disease remains a public health problem in Korea. Here we report the outbreaks and surveillance of animal rabies in Gangwon-do. Animal rabies infections were identified in 119 animals from 1993 to 2003. The $78\%$ of all rabid animals were domestic species in Gangwon-do. Wild Korean raccoon dog (N. p. koreensis) continued to be the only reported rabid wildlife species. Outbreaks of rabies infections in Korean raccoon dogs are found in broad geographic regions across the northern Gangwon-do. The principal rabies hosts today are probably wild animals in Gangwon-do. The malaise, cerebral dysfunction, anxiety, confusion, agitation and abnormal behavior of the animals were the important symptoms of the disease. The Encephalitis, infiltration with lymphocytes and polymorphonuclear leukocytes and the inclusion bodies (Negri bodies) in neuronal cells were the specific histopathological signs. The results of indirect fluorescent antibody test (IFA) for animal rabies diagnosis were identical and the technique was useful to diagnose the disease. Preexposure vaccination is recommended for persons in high-risk groups, such as laboratory workers, veterinarians and certain animal handlers.

• Integrative Medicine Research
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• v.3 no.1
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• pp.4-10
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• 2014

Green tea and coffee consumption have been widely popular worldwide. These beverages contain caffeine to activate the central nervous system by adenosine receptor blockade, and due to the caffeine, addiction or tolerance may occur. In addition to this caffeine effect, green tea and coffee consumption have always been at the center of discussions about human health, disease, and longevity. In particular, green tea catechins are involved in many biological activities such as antioxidation and modulation of various cellular lipid and proteins. Thus, they are beneficial against degenerative diseases, including obesity, cancer, cardiovascular diseases, and various inflammatory diseases. Some reports also suggest that daily consumption of tea catechins may help in controlling type 2 diabetes. However, other studies have reported that chronic consumption of green tea may result in hepatic failure, neuronal damage, and exacerbation of diabetes, suggesting that interindividual variations in the green tea effect are large. This review will focus on the effect of green tea catechins extracted from the Camellia sinensis plant on type 2 diabetes and obesity, and the possible mechanistic explanation for the experimental results mainly from our laboratory. It is hoped that green tea can be consumed in a suitable manner as a supplement to prevent the development of type 2 diabetes and obesity.

• Journal of Veterinary Clinics
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• v.36 no.3
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• pp.180-183
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• 2019

A 7-year-old, male Maltese dog with a body weight of 2.8 kg was presented with a history of hind limbs ataxia that progressed to tetraparesis over a one-month period. Based on physical and neurological examinations, tetraparesis with concomitant UMN signs, kyphosis and severe neck pain were identified. On MRI scan, we tentatively diagnosed this patient as a primary intramedullary spinal cord tumor. Therapy with lomustine plus hydroxyurea and prednisolone was initiated and the clinical signs rapidly improved. The patient was regularly checked by MRI scan and the range of the mass was gradually reduced to complete remission for 11 months. About 19 months after treatment, the patient showed anemia and hematochezia which suspected as adverse effects of chemotherapy. The condition was getting worse over 2 months and the patient suddenly expired 657 days after initial presentation. On histopathological examination, the spinal cord sample was identified as a neuronal atrophy without evidence of tumor cell.

• Microbiology and Biotechnology Letters
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• v.50 no.1
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• pp.157-163
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• 2022

Alcoholic liver disease (ALD), which encompasses alcoholic steatosis, alcoholic hepatitis, and alcoholic cirrhosis, is a major cause of morbidity and mortality worldwide. Although the economic and health impacts of ALD are clear, few advances have been made in its prevention or treatment. We recently demonstrated that the insect-derived antimicrobial peptide CopA3 exerts anti-apoptotic and anti-inflammatory activities in various cell systems, including neuronal cells and colonic epithelial cells. Here, we tested whether CopA3 inhibits ethanol-induced liver injury in mice. Mice were intraperitoneally injected with ethanol only or ethanol plus CopA3 for 24 h and then liver injury and inflammatory responses were measured. Ethanol enhanced the production of proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interferon (IFN)-γ, and IL-10. It also induced hepatocyte apoptosis and ballooning degeneration in hepatocytes. Notably, all these effects were eliminated or significantly reduced by CopA3 treatment. Collectively, our findings demonstrate that CopA3 ameliorates ethanol-induced liver cell damage and inflammation, suggesting the therapeutic potential of CopA3 for treating ethanol-induced liver injury.

• IMMUNE NETWORK
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• v.23 no.1
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• pp.7.1-7.27
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• 2023

The mammalian intestines harbor trillions of commensal microorganisms composed of thousands of species that are collectively called gut microbiota. Among the microbiota, bacteria are the predominant microorganism, with viruses, protozoa, and fungi (mycobiota) making up a relatively smaller population. The microbial communities play fundamental roles in the maturation and orchestration of the immune landscape in health and disease. Primarily, the gut microbiota modulates the immune system to maintain homeostasis and plays a crucial role in regulating the pathogenesis and pathophysiology of inflammatory, neuronal, and metabolic disorders. The microbiota modulates the host immune system through direct interactions with immune cells or indirect mechanisms such as producing short-chain acids and diverse metabolites. Numerous researchers have put extensive efforts into investigating the role of microbes in immune regulation, discovering novel immunomodulatory microbial species, identifying key effector molecules, and demonstrating how microbes and their key effector molecules mechanistically impact the host immune system. Consequently, recent studies suggest that several microbial species and their immunomodulatory molecules have therapeutic applicability in preclinical settings of multiple disorders. Nonetheless, it is still unclear why and how a handful of microorganisms and their key molecules affect the host immunity in diverse diseases. This review mainly discusses the role of microbes and their metabolites in T helper cell differentiation, immunomodulatory function, and their modes of action.

• Biomolecules & Therapeutics
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• v.32 no.5
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• pp.531-539
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• 2024

Sleep is one of the most essential physiological phenomena for maintaining health. Sleep disturbances, such as insomnia, are often accompanied by psychiatric or physical conditions such as impaired attention, anxiety, and stress. Medication used to treat insomnia have concerns about potential side effects with long-term use, so interest in the use of alternative medicine is increasing. In this study, we investigated the hypnotic effects of β-lapachone (β-Lap), a natural naphthoquinone compound, using pentobarbital-induced sleep test, immunohistochemistry, real-time PCR, and western blot in mice. Our results indicated that β-Lap exerts a significant hypnotic effect by showing a decrease in sleep onset latency and an increase in total sleep time in pentobarbital-induced sleep model. The results of c-Fos immunostaining showed that β-Lap decreased neuronal activity in the basal forebrain and lateral hypothalamus, which are wakefulness-promoting brain regions, while increasing in the ventrolateral preoptic nucleus, a sleep-promoting region; all these effects were significantly abolished by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A₁ receptor (A₁R) antagonist. Western blot analysis showed that β-Lap increased extracellular signal-regulated kinase phosphorylation and nuclear factor-kappa B translocation from the cytoplasm to the nucleus; these effects were inhibited by DPCPX. Additionally, β-Lap increased the mRNA levels of A₁R. Taken together, these results suggest that β-Lap exerts hypnotic effects, potentially through A₁R.

• The Korean Journal of Pain
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• v.37 no.4
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• pp.299-309
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• 2024

Chronic peripheral neuropathic pain therapy currently focuses on modulating neuroinflammatory conditions. Methylcobalamin (MeCbl), a neuroregenerative agent, modulates neuroinflammation. This review aimed to explore the molecular pharmacology action of MeCbl as a chronic peripheral neuropathic pain therapeutic agent. MeCbl plays a role in various cellular processes and may have therapeutic potential in neurodegenerative diseases. Intracellular MeCbl modulates inflammation by regulating the activity of T lymphocytes and natural killer cells as well as secretion of inflammatory cytokines, namely, tumor necrosis factor-α, interleukin-6, interleukin-1β, epidermal growth factor, and neuronal growth factor. MeCbl can reduce pain symptoms in chronic neuropathic pain conditions by decreasing excitation and hyperpolarization-induced ion channel activity in medium-sized dorsal root ganglion (DRG) neurons and the expression of transient receptor potential ankyrin 1, transient receptor potential cation channel subfamily M member 8, phosphorylated p38MAPK, transient receptor potential cation channel subfamily V members 1 and 4 in the DRG, and the voltage-gated sodium channel in axons.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.3
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• pp.279-286
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• 2016

Caffeic acid phenethyl ester (CAPE), derived from honeybee hives, is a bioactive compound with strong antioxidant activity. This study was designed to test the neuroprotective effect of CAPE in 3-nitropropionic acid (3NP)-induced striatal neurotoxicity, a chemical model of Huntington's disease (HD). Initially, to test CAPE's antioxidant activity, a 2,2'-azino-bis-3-ethylbenzthiazoline-6-sulfonic acid (ABTS) antioxidant assay was employed, and CAPE showed a strong direct radical-scavenging effect. In addition, CAPE provided protection from 3NP-induced neuronal cell death in cultured striatal neurons. Based on these observations, the in vivo therapeutic potential of CAPE in 3NP-induced HD was tested. For this purpose, male C57BL/6 mice were repeatedly given 3NP to induce HD-like pathogenesis, and 30 mg/kg of CAPE or vehicle (5% dimethyl sulfoxide and 95% peanut oil) was administered daily. CAPE did not cause changes in body weight, but it reduced mortality by 29%. In addition, compared to the vehicle-treated group, robustly reduced striatal damage was observed in the CAPE-treated animals, and the 3NP-induced behavioral deficits on the rotarod test were significantly rescued after the CAPE treatment. Furthermore, immunohistochemical data showed that immunoreactivity to glial fibrillary acidic protein (GFAP) and CD45, markers for astrocyte and microglia activation, respectively, were strikingly reduced. Combined, these data unequivocally indicate that CAPE has a strong antioxidant effect and can be used as a potential therapeutic agent against HD.