• Journal of Microbiology and Biotechnology
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• 제29권4호
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• pp.645-650
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• 2019

Brown adipocytes have an important role in the regulation of energy balance through uncoupling protein-1 (UCP-1)-mediated nonshivering thermogenesis. Although brown adipocytes have been highlighted as a new therapeutic target for the treatment of metabolic diseases, such as obesity and type II diabetes in adult humans, the molecular mechanism underlying brown adipogenesis is not fully understood. We recently found that protein tyrosine phosphatase receptor type B (PTPRB) expression dramatically decreased during brown adipogenic differentiation. In this study, we investigated the functional roles of PTPRB and its regulatory mechanism during brown adipocyte differentiation. Ectopic expression of PTPRB led to a reduced brown adipocyte differentiation by suppressing the tyrosine phosphorylation of VEGFR2, whereas a catalytic inactive PTPRB mutant showed no effects on differentiation and phosphorylation. Consistently, the expression of brown adipocyte-related genes, such as UCP-1, $PGC-1{\alpha}$, PRDM16, $PPAR-{\gamma}$, and CIDEA, were significantly inhibited by PTPRB overexpression. Overall, these results suggest that PTPRB functions as a negative regulator of brown adipocyte differentiation through its phosphatase activity-dependent mechanism and may be used as a target protein for the regulation of obesity and type II diabetes.

• Journal of Ginseng Research
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• 제47권2호
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• pp.228-236
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• 2023

Background: QiShen YiQi pills (QSYQ) is a Traditional Chinese Medicine (TCM) formula, which has a significant effect on the treatment of patients with myocardial infarction (MI) in clinical practice. However, the molecular mechanism of QSYQ regulation pyroptosis after MI is still not fully known. Hence, this study was designed to reveal the mechanism of the active ingredient in QSYQ. Methods: Integrated approach of network pharmacology and molecular docking, were conducted to screen active components and corresponding common target genes of QSYQ in intervening pyroptosis after MI. Subsequently, STRING and Cytoscape were applied to construct a PPI network, and obtain candidate active compounds. Molecular docking was performed to verify the binding ability of candidate components to pyroptosis proteins and oxygen-glucose deprivation (OGD) induced cardiomyocytes injuries were applied to explore the protective effect and mechanism of the candidate drug. Results: Two drug-likeness compounds were preliminarily selected, and the binding capacity between Ginsenoside Rh2 (Rh2) and key target High Mobility Group Box 1 (HMGB1)was validated in the form of hydrogen bonding. 2 μM Rh2 prevented OGD-induced H9c2 death and reduced IL-18 and IL-1β levels, possibly by decreasing the activation of the NLRP3 inflammasome, inhibiting the expression of p12-caspase1, and attenuating the level of pyroptosis executive protein GSDMD-N. Conclusions: We propose that Rh2 of QSYQ can protect myocardial cells partially by ameliorating pyroptosis, which seems to have a new insight regarding the therapeutic potential for MI.

• Advances in Traditional Medicine
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• 제5권4호
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• pp.251-261
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• 2005

Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder with a complex genetic component. RA is characterized by chronic inflammation of the synovial membrane in the joint, which leads to the progressive destruction of articular cartilage, ligament and bone. Several cytokines such as tumor necrosis $factor-{\alpha}\;TNF-{\alpha}\;and\;interleukin-1{\beta}\;(IL-1{\beta})$ and interleukin-6 (IL-6) have been implicated in the pathological mechanisms of synovial tissue proliferation, joint destruction and programmed cell death in rheumatoid joint. Genome wide screening of subjects suffering from autoimmune diseases especially arthritis revealed linkage to inflammatory molecules like $TNF-{\alpha},\;IL-1{\beta}$ and IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappaB $(NF-{\kappa}B)$ and human leucocyte antigen/major histocompatibility complex (HLA/MHC) locus. The status of the pharmacological mechanism of herbal drugs in the light of genome wide screening results has been discussed to reinforce the therapeutic potential and the pharmacological basis of the herbal drugs.

• Journal of Ginseng Research
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• 제27권3호
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• pp.115-119
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• 2003

There has been continuing interest in the development of synthetic and natural compounds that modify the immune response particularly for the treatment of AIDS and cancer. During the past fifty years, numerous scientific studies have been published on ginseng. Modem human studies have investigated preventive effect of ginseng on several kinds of cancer, its long term immunological effect on HIV patients, its effect on cell mediated immune functions in healthy volunteers. Similarly non clinical studies on animal model system have studied the chemopreventive action of ginseng on cancer and immunological properties of ginseng. The precise mechanism of action of ginseng, however, not clearly understood. Considering its wide-ranging therapeutic effects, this study is being undertaken to elucidate the general mode of action of ginseng, especially to test our hypothesis that its biological action may be mediated by the immune system.

• 생물정신의학
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• 제2권2호
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• pp.157-168
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• 1995

The neuropsychiatric sequelae of traumatic brain unjury(TBI) are effects on complex aspect of behavior, cognition and emotional expression. They include psychiatric disorders such as depression, psychosis, personality change, dementia, and postconcussion syndrome. The damage is done not only to the cortex of the brain but also to subcortical and axial structures. The diffuse degeneration of cerebral white mailer is axonal damage that is caused by mechanical forces shearing the neuronal fiber at the moment of impact(diffuse axonal injury, DAI). The DAI and the changed receptor-agonist mechanism ore the most important mechanisms in genesis of neuropsychiatric sequalae by mild TBI. The most important instrument for diagnosis of neuropsychiatric sequalae of TBI is a physician or psychiatrist with experience and knowledge. The most effective therapeutic tool is a professional who understands the nature of the problem.

• Annals of Clinical Neurophysiology
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• 제13권1호
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• pp.26-30
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• 2011

Although the pathophysiologic mechanism is unknown, there has been long-running debate on whether periodic discharges such as periodic lateralized epileptiform discharges (PLEDs) and generalized periodic epileptiform discharges are an ictal or interictal EEG pattern. The goal of this review is to give evidence that such periodic discharges on EEG are not ictal phenomenon and just represent underlying acute brain damage. This review includes coma with epileptiform EEG pattern and its prognostic and therapeutic implications. Based on previous reports, rather than taking the view PLEDs represent either an underlying ictal process or an electrographic correlate of neuronal injury, it would be more reasonable that PLEDs are considered as a dynamic pathophysiological state in which unstable neurobiological processes create an ictal-interictal continuum.

• 한국발생생물학회지:발생과생식
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• 제16권3호
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• pp.155-168
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• 2012

Therapeutic cancer is a long lasting and turbulent history accompany with the milestones in surgical intervention, chemotherapy and radiotherapy. In the past decade, however, metastatic cancer still obstinately exists challenging the professional scientist. Beside the major forms of cancer treatment, Diphtheria toxin (DT) which is produced by a pathogenic strain of bacterium Corynebacterium diphtheria to shield themselves against the other dangerous organism, have been researched as a potential candidate to overcome the drawback such as non-specific, non-effect to drug resistant cancer cell and side effects when using chemotherapy and radiotherapy. In the context of suicide gene therapy, the DT expression under controlling of tissue-specific promoter will be targeted in cancer cell but defect in normal cell. The molecular mechanism, characteristic of DT-bases therapy and prominent achievements of preclinical and clinical studies for the past decade are summarized and discussed in this review.

• IMMUNE NETWORK
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• 제1권2호
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• pp.95-103
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• 2001

T cells play a central role in the initiation and regulation of the immune response to foreign antigens. Full activation of T cells requires the engagement of T cell receptor complex (TCR) and the binding of a second costimulatory receptor to its ligand expressed on antigen presenting cells (APC). Among the molecules known to provide costimulatory function, CD28 has been the most dominant and potent costimulatory molecule. However, the function of CD28 is becoming more complex due to the recent discovery of its structural homologue, CTLA-4 and ICOS. This review summarizes the biology and physiologic function of each of these receptors, and further focuses on the biochemical mechanism underlying the function of these receptors. Complete understanding of the CD28/CTLA-4/ICOS costimulatory pathway will provide the basis for developing new therapeutic approaches for immunological dieseases.

• 생물정신의학
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• 제24권4호
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• pp.175-187
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• 2017

Transcranial direct current stimulation (TDCS) is a clinically safe and effective method of delivering weak electric current to modulate cortical activities. And based on the cumulating scientific evidences, the method is recommended to treat major depressive disorder (MDD) and other psychiatric disorders. In this paper, we review the development of TDCS in the rising field of neuromodulation. Then with suggested biochemical and physical mechanism of TDCS, we summarize the reported cases of using TDCS to alleviate major neuropsychiatric disorders. And, in particular, the treatment of MDD is highlighted as an illustrative example of using TDCS. We discuss here the therapeutic potentials of this method in psychiatry. And in closing remarks, we evaluate the current technical limitations and suggest the future directions of this method in both the clinical and research aspects.

• BMB Reports
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• 제50권8호
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• pp.401-410
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• 2017

The protein disulfide isomerase (PDI) family is a group of multifunctional endoplasmic reticulum (ER) enzymes that mediate the formation of disulfide bonds, catalyze the cysteine-based redox reactions and assist the quality control of client proteins. Recent structural and functional studies have demonstrated that PDI members not only play an essential role in the proteostasis in the ER but also exert diverse effects in numerous human disorders including cancer and neurodegenerative diseases. Increasing evidence suggests that PDI is actively involved in the proliferation, survival, and metastasis of several types of cancer cells. Although the molecular mechanism by which PDI contributes to tumorigenesis and metastasis remains to be understood, PDI is now emerging as a new therapeutic target for cancer treatment. In fact, several attempts have been made to develop PDI inhibitors as anti-cancer drugs. In this review, we discuss the properties and diverse functions of human PDI proteins and focus on recent findings regarding their roles in the state of diseases including cancer and neurodegeneration.