• 생명과학회지
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• 제34권3호
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• pp.199-207
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• 2024

CYP 효소는 내인성 및 외인성 화학물질의 대사에 핵심적인 역할을 담당한다. 특히, 약물, 자연생성물 및 환경 독성 화학물질 등은 조직에 따라 특이적 CYP 효소 유전자의 발현을 조절하며, 이는 체내 유입된 약물과 독성물질 등과 같은 화학물질들 사이의 상호작용을 유발하여 이들의 대사에 영향을 줌으로써, 결국 치료 효과와 독성 효과에 변화를 초래한다. 이 분야에 대한 지난 수십 년 동안의 집중적인 연구는, 이러한 CYP 효소 유전자의 발현조절을 매개하는 분자적 기전을 이해하는 데 상당한 진전을 가져왔다. 이제는 구체적인 CYP 효소 유전자의 발현 유도를 조절하는 화합물들뿐만 아니라, 이를 감지하여 특정 CYP 유전자의 발현 조절을 매개하는 데 관여하는 수용체들과 이들의 신호전달 경로들이 비교적 상세히 밝혀졌다. 본 총설에서는, 다양한 화학물질의 노출에 반응하여 CYP 효소 유전자들의 발현 유도를 매개하는 것으로 알려진 주요 외인성 물질-감지 수용체들과 기타 조절인자들의 분자적 작용기전을 요약한다.

• Journal of Korean Neurosurgical Society
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• 제62권4호
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• pp.487-491
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• 2019

Conservative therapy with appropriate antibiotics is essential for most patients with infectious spondylitis. Although most antibiotics do not cause problems if it used properly and serious side effects are rare, side effects can occur with any class of drugs and adverse reactions of antibiotics can range from mild allergic reactions to serious and fulminant adverse events. These side effects are also extremely variable from patient to patient and from antibiotic to antibiotic. A side effect of antibiotics may paradoxically increase inflammatory marker levels. Here, the author presents two cases of antibiotic-induced increase in inflammatory markers in cured infectious spondylitis. The patients were successfully treated after stopping the antibiotic therapy. The differential diagnosis between antibiotic side effects and infection should be considered very carefully because the treatment is completely different. Although the exact mechanisms underlying successful treatment without antibiotics are unclear, we should consider the side effects of antibiotics when following inflammatory markers during treatment of infectious spondylitis.

• Journal of Ginseng Research
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• 제44권1호
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• pp.24-32
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• 2020

Cardiovascular diseases prevail among modern societies and underdeveloped countries, and a high mortality rate has also been reported by the World Health Organization affecting millions of people worldwide. Hyperactive platelets are the major culprits in thrombotic disorders. A group of drugs is available to deal with such platelet-related disorders; however, sometimes, side effects and complications caused by these drugs outweigh their benefits. Ginseng and its nutraceuticals have been reported to reduce the impact of thrombotic conditions and improve cardiovascular health by antiplatelet mechanisms. This review provides (1) a comprehensive insight into the available pharmacological options from ginseng and ginsenosides (saponin and nonsaponin fractions) for platelet-originated cardiovascular disorders; (2) a discussion on the impact of specific functional groups on the modulation of platelet functions and how structural modifications among ginsenosides affect platelet activation, which may further provide a basis for drug design, optimization, and the development of ginsenoside scaffolds as pharmacological antiplatelet agents; (3) an insight into the synergistic effects of ginsenosides on platelet functions; and (4) a perspective on future research and the development of ginseng and ginsenosides as super nutraceuticals.

• Journal of Yeungnam Medical Science
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• 제29권2호
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• pp.77-82
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• 2012

AMP-activated protein kinase (AMPK) is an important cellular fuel sensor. Its activation requires phosphorylation at Thr-172, which resides in the activation loop of the ${\alpha}1$ and ${\alpha}2$ subunits. Several AMPK upstream kinases are capable of phosphorylating AMPK at Thr-172, including LKB1 and CaMKK${\beta}$ ($Ca^{2+}$/calmodulin-dependent protein kinase kinase${\beta}$). AMPK has been implicated in the regulation of physiological signals, such as in the inhibition of cholesterol fatty acid, and protein synthesis, and enhancement of glucose uptake and blood flow. AMPK activation also exhibits several salutary effects on the vascular function and improves vascular abnormalities. AMPK is modulated by numerous hormones and cytokines that regulate the energy balance in the whole body. These hormone and cytokines include leptin, adiponectin, ghrelin, and even thyroid hormones. Moreover, AMPK is activated by several drugs and xenobiotics. Some of these are in being clinically used to treat type 2 diabetes (e.g., metformin and thiazolidinediones), hypertension (e.g., nifedipine and losartan), and impaired blood flow (e.g., aspirin, statins, and cilostazol). I reviewed the precise mechanisms of the AMPK activation pathway and AMPK-modulating drugs.

• 대한약리학회지
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• 제11권1호
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• pp.55-60
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• 1975

An animal which is placed in a new environment displays a complex behavioral pattern consisting of locomotion, grooming and rearing. This behavioral pattern is influenced by endogenous and exogenous stimuli, such as hormonal secretion, level of neurohumoral transmitters, drugs and light. It is widely known that the most tranquilizers depressed spontaneous motor activity although their mechanisms of action were different, while antidepressants stimulated except imipramine which showed various action. Until the present time, the hole-board apparatus, which gives rather subjective data, has been used extensively to study the effects of drugs on general activity and exploratory behavior in mice. Recently a new apparatus for mobility measurements, called a 'Selective Activity Meter' has been introduced. This instrument supposedly produces more objective data on activity and behavior. The purpose of the present experiment was to study the influence of psychotropics on motor activity using the Selective Activity Meter. In the experiment, various psychotropic agents such as major tranquilizers(chlorpromazine, haloperidol); minor tranquilizers(meprobamate, diazepam); and antidepressants(amphetamine, imipramine) were used. In each experiment, the drug was administered to five mice and their activity was recorded. Each experiment was run five or more times and the results are based on the mean of each trial. The results are summarized as follows: 1. The group of mice treated with chlorpromazine showed markedly inhibited motor activity in comparison with controls and the inhibitory action of chlorpromazine was shown to be more intense than any of the other drugs used in the test. Haloperidol administration yielded similar results until 60 minutes, but mice showed less inhibition of motor activity than with chlorpromazine after 90 minutes. 2. In the group treated with diazepam, there was strong inhibition of motor activity until 30 minutes, but after 60 minutes the mice showed less inhibition than with chlorpromazine. In the meprobamate group, motor activity was inhibited in a manner similar to that of other tranquilizers, but the inhibition was less than that of diazepam. 3. In the group treated with imipramine, the inhibition developed gradually after ten minutes. 4. The effects of amphetamine did not appear until 30 minutes after administration, but then there was a significant increase in the motor activity.

• 대한의생명과학회지
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• 제18권4호
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• pp.345-354
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• 2012

Angelica keiskei has exhibited numerous pharmacological effects including antitumor, antimetastatic, and antidiabetic effects. However, the anti-inflammatory effects and mechanisms employed by xanthoangelol E isolated from Angelica keiskei are incompletely understood. In this study, we attempted to determine the effects of Xanthoangelol E on the lipopolysaccharide (LPS)-stimulated mouse peritoneal macrophage. The findings of this study demonstrated that xanthoangelol E inhibited the production of tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-6, and prostaglandin $E_2$ ($PGE_2$). Xanthoangelol E inhibited the enhanced levels of cyclooxygenase (COX)-2 and inducible nitric oxide synthase (iNOS) caused by LPS. Additionally, we showed that the anti-inflammatory effect of xanthoangelol E is through the regulation of the activation of nuclear factor (NF)-${\kappa}B$ and caspase-1. These results provide novel insights into the pharmacological actions of xanthoangelol E as a potential candidate for the development of new drugs to treat inflammatory diseases.

• Journal of Dental Anesthesia and Pain Medicine
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• 제15권1호
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• pp.1-4
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• 2015

In pediatric dentistry, chloral hydrate is habitually selected for sedation of uncooperative children. Although chloral hydrate has been used for decades, various adverse effects are reported and necessity for new alternative drugs has increased. Dexmedetomidine was approved by FDA for sedation at intensive care units (ICU) in 1999. Compared to conventional sedative drugs, dexmedetomidine has not only analgesic and sedative effects but also it barely suppresses the respiratory system. Due to these characteristics, dexmedetomidine is known as safe sedative drug for children and elderly patients. Furthermore, approved by KFDA in 2010 in Korea, the frequency of sedation using dexmedetomidine is increasing. However, due to its intravenous administration method, it was difficult to apply in pediatric dentistry. Recently, intranasal administration method was introduced which might be a new possible alternative of oral sedation. In this study, we compare the mechanisms, pros and cons of chloral hydrate and dexmedetomidine, introducing new possibilities.

• 정신신체의학
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• 제21권2호
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• pp.81-92
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• 2013

새로운 항우울제가 개발되고 임상에서 정신과적 질환뿐만이 아니라 만성통증증후군, 섬유근통증증후군, 두통 등의 많은 정신신체질환 그리고 신체질환자의 적응장애 및 우울증 등의 자문조정정신의학 영역에서도 다양하게 자주 사용되고 있다. 다양한 정신의학적 질환을 치료하기 위해 처방하는 새로운 항우울제의 사용 시 치료중단의 가장 큰 원인은 약물부작용이다. 이 논문은 현재 우리나라에서 널리 사용되고 있는 새로운 항우울제 사용 시 나타나는 부작용들 중 정신신체의학과 자문조정정신의학영역에서 관심을 가져야 할 매우 빈번하게 나타나는 세 가지 부작용인 오심과 구토, 체중증가, 성기능장애에 대한 발생기전, 발생빈도, 그리고 약물학적 처치를 위주로 한 해결방안을 알아보았다. 저자는 이 논문을 통하여 정신건강의학과 의사만이 아니라 정신신체의학 영역에 관심을 가지거나 자문조정정신의학과 연계되는 타과 영역의 의사들이 새로운 항우울제를 사용할 때 빈번하게 나타나서 삶의 질을 떨어뜨리고 치료중단을 일으킬 수 있는 이 약물들의 부작용을 잘 인지함으로써 이를 조기에 발견하고 적절히 해결하여 환자 치료에 도움을 주고자 하였다.

• 대한한의학방제학회지
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• 제10권1호
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• pp.157-167
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• 2002

This study was performed to investigate what effect the taste and quality of drugs would have on the cold and heat mechanisms of human body. We administered Hwangryeunhaedok-tang composed of bitter-tasted, cold-qualified drugs and Gungangbuza-tang composed of spice-tasted. hot-qualified drugs, respectively to the mice 1 hr before exposure to heat stress or cold stress. Plasma corticosterone level of mice was measured. The results were as follows: 1. The elevated corticosterone level in the mice exposed to heat stress was significantly decreased after administration of Gungangbuza-tang but there was no decrease after administration of Hwangryeunhaedok-tang. 2. The elevated corticosterone level in the mice exposed to cold stress was significantly decreased after administration of Hwangryeunhaedok-tang but there was mild decrease after administration of Gungangbuza-tang. 3. When the doses, 3g/kg and 1g/kg were administerd to mice exposed to heat stress. both dose showed significant decrease of corticosterone level and the dose. 3g/kg was more effective. However, in the mice exposed to cold stress, the dose, 3g/kg showed mild decrease and 1g/kg showed significant decrease. These data suggested that HW decreased the plasma corticosterone level in the mice exposed to cold stress and GB also decreased the plasma corticosterone level in the mice exposed to heat stress. In conclusion, our study revealed that the taste and quality of drugs controled the cold and heat mechanism of human body.

• The Korean Journal of Pain
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• 제22권1호
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• pp.1-15
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• 2009

Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.