• Journal of Korean Neurosurgical Society
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• v.57 no.4
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• pp.307-310
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• 2015

We report a case of a paradoxical response of a tuberculoma in the brain mimicking a brain tumor. A 76-year-old woman presented with a 2 week history of headache, dysarthia, and orthopnea. Brain magnetic resonance images (MRI) revealed two rim-enhancing lesions on the pons and occipital lobe, and chest computed tomography showed randomly distributed miliary nodules. The tentative diagnosis was tuberculosis (TB) of the brain and lung. She complained of right hemiparesis and worsening general weakness after taking the anti-TB medication. On the monthly follow-up images, the enhanced lesions were enlarged with increased perfusion and choline/creatinine ratio, suggesting a high grade glioma. A surgical resection was completed to diagnose the occipital lesion, and the tuberculoma was pathologically confirmed by a positive TB-polymerase chain reaction. The anti-TB medication was continued for 13 months. A follow-up MRI showed decreased size of the brain lesions associated with perilesional edema, and the clinical symptoms had improved. Brain tuberculoma could be aggravated mimicking brain malignancy during administration of anti-TB medication. This paradoxical response can be effectively managed by continuing the anti-TB drugs.

• The Journal of Korean Medicine
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• v.21 no.2
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• pp.52-59
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• 2000

Objectives: The root and stem of Sinomenium acutum has been used for treatment of arthritis and neuralgia in oriental medicine. To find new substances of the anti-anaphylactic drugs, we studied Sinomenium acutum. Methods: To investigate the effect of this plant, the effect on anaphylactic reaction, plasma histamine level, and tumor necrosis $factor-{\alpha}-(TNF-{\alpha})$ production were measured after the aqueous extract of Sinomenium acutum stem (SSAE) was administrated to mice and rats. Results: The SSAE (0.1 to 1000 mg/kg) dose-dependently inhibited systemic anaphylactic reaction induced by compound 48/80 in mice. Especially, SSAE reduced compound 48/80-induced anaphylactic reaction with 50% at the dose of 1000 mg/kg. SSAE (100 to 1000 mg/kg) also significantly inhibited local anaphylactic reaction activated by anti-dinitrophenyl (DNP) IgE. When mice were pretreated with SSAE at a concentration ranging from 0.1 to 1000 mg/kg, the plasma histamine levels were reduced in a dose-dependent manner. SSAE (1 to 1000 g/ml) dose-dependently inhibited histamine release from the rat peritoneal mast cells (RPMCs) activated by compound 48/80 or anti-DNP IgE. The level of cAMP in RPMCs, when SSAE was added, increased compared with that of a normal control. In addition, SSAE (0.1 g/ml) had a significant inhibitory effect on anti-DNP IgE-induced $TNF-{\alpha}$ production. Conclusions: These results indicate that SSAE inhibits mast cell-mediated anaphylactic reactions and $TNF-{\alpha}$ production from mast cells.

• Biomedical Science Letters
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• v.18 no.4
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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.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.260.1-260.1
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• 2002

Green tea contains several antioxidants including polyphenols of the catechin. which have been shown to act in vitro and in vivo as anti-inflammatory. anti-viral and anti-tumor drugs. Prostaglandins (PGs) are a family of intercellular and intracellular messengers derived from arachidonic acid(AA) by phospholipase(PL) and cyclooxygenase(COX). These mediators exert a wide range of effects on processes such as smooth muscle tone. vascular permeability, cellular proliferation. and inflammatory/immune function. (omitted)

• Journal of Plant Biotechnology
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• v.50
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• pp.27-33
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• 2023

Zizyphus jujube is a plant in the buckthorn family (Rhamnaceae) that has been the subject of research into antibacterial, antifungal and anti-inflammatory properties of its fruit and seed. However, few studies have investigated its leaves. In this study, the anti-inflammatory activity of ZJL (an extract of Z. jujube leaf) was evaluated to verify its potential as an anti-inflammatory agent and SARS-CoV-2 medicine, using nitric oxide (NO) assay, RT-PCR, SDSPAGE, Western blotting, and UHPLC/TOFHRMS analysis. We found that ZJL suppresed pro-inflammatory mediators such as NO, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and tumor necrosis factor α (TNF-α) in lipopolysaccharide (LPS)-induced RAW264.7 cells. ZJL acted by inhibiting NF-KB and MAPK signaling pathway activity. We also confirmed that ZJL contains a phenol compound and flavonoids with anti-inflammatory activity such as trehalose, maleate, epigallocatechin, hyperoside, catechin, 3-O-coumaroylquinic acid, rhoifolin, gossypin, kaempferol 3-neohesperidoside, rutin, myricitrin, guaiaverin, quercitrin, quercetin, ursolic acid, and pheophorbide a. These findings suggest that ZJL may have great potential for the development of anti-inflammatory drugs and vaccines via inhibition of NF-κB and MAPK signaling in LPS-induced RAW264.7 cells.

• The Korea Journal of Herbology
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• v.34 no.2
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• pp.49-58
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• 2019

Objectives : Obesity is a public health concern associated with chronic diseases including hyperlipidemia, diabetes, fatty liver, atherosclerosis and cancer. As several anti-obesity drugs have been limited owing to their side effects, the development of new anti-obesity drugs through herbal medicines has been increasing. Cynanchum Wilfordii Radix (CW) traditionally is consumed for various health benefits including immune enhancing, anti-inflammation and anti-tumor activities. The aim of the present study is to evaluate the effects of CW on High fat diet (HFD)-induced obese mice. Methods : The mice were randomly divided into four groups (n=7). The mice were respectively fed a normal diet (ND), a high-fat diet (HFD), HFD plus CW (50 mg/kg/day), HFD plus CW (100 mg/kg/day). All groups were assayed for body weights, food efficiency ratio, blood biochemistry parameters, and organic tissue weights. Results : HFD-fed mice showed an increase in the body weight and serum biochemistry parameters levels (total cholesterol and triglycerides) as well as organic tissue weights. However, the administration of CW to obese mice induced a reduction in their body weight, food efficiency ratio, blood biochemistry parameters and weight of liver and fat compared with the HFD fed mice. Additionally, we observed that CW inhibited the lipid accumulation in liver and serum lipid parameter induced by HFD. Conclusions : Taken together, the findings of this study suggest that CW may be a potential agent for use in the treatment of obesity and obesity-related metabolic diseases.

• Journal of Life Science
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• v.21 no.11
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• pp.1641-1651
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• 2011

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL/Apo2L) is a recently identified member of the TNF ligand family that can initiate apoptosis through the activation of their death receptors. TRAIL has been paid attention as a potential anti-cancer drug, because it selectively induces apoptosis in tumor cells in vitro and in vivo but not in most normal cells. However, recent studies have shown that some cancer cells including malignant renal cell carcinoma and hepatocellular carcinoma, are resistant to the apoptotic effects of TRAIL. Therefore, single treatment with TRAIL may not be sufficient for the treatment of various malignant tumor cells. Understanding the molecular mechanisms of TRAIL resistance and identification of sensitizers capable of overcoming TRAIL resistance in cancer cells is needed for the establishment of more effective TRAIL-based cancer therapies. Chemotherapeutic drugs induce apoptosis and the upregulation of death receptors or activation of intracellular signaling pathways of TRAIL. Numerous chemotherapeutic drugs have been shown to sensitize tumor cells to TRAIL-mediated apoptosis. In this study, we summarize biological agents and drugs that sensitize tumors to TRAIL-mediated apoptosis and discuss the potential molecular basis for their sensitization.

• The Journal of Internal Korean Medicine
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• v.29 no.2
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• pp.490-499
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• 2008

Objectives : This study was aimed to elucidate the effects of Trichosanthes kirilowii extract (TKE) on the angiogenesis and growth of tumor cells. Methods : Tube formation assay was performed by using human umbilical vein endothelial cells (HUVEC), and anchorage dependent colony assay was performed by using B16-F10 melanoma, Hep G2 and HT1080, CT-26 and SNU-1 cells. Results : For HUVEC, TKE at a level of more than 100 ${\mu}g/m{\ell}$ suppresses cell growth. For HUVEC at 100 ${\mu}g/m{\ell}$ and greater TKE density, the formation of tubes was suppressed in a dose-dependant manner. TKE controls the colony formations of B16-F10 melanoma cells, CT 26 cells, and Hep G2 cells, and its effect is proportional to density. In HT1080 cells and SNU-1 cells, formation is suppressed regardless of density. Conclusions : From these results, it could be concluded that TKE has significant properties on anti-angiogenesis and growth inhibiting of tumor cells. It is suggested that TKE will be a good candidate for new drugs or therapeutics for anti-angiogenesis.

• Macromolecular Research
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• v.17 no.2
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• pp.99-103
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• 2009

We evaluated the efficacy of pH-sensitive micelles, formed by methoxy poly(ethylene glycol)-b-poly($\beta$)-amino ester) (PEG-PAE), as carriers for paclitaxel (PIX), a drug currently used to treat various cancers. PTX was successful encapsulated by a film hydration method. Micelles encapsulated more than 70% of the PTX and the size of the PTX-encapsulated micelles (PTX-PM) was less than 150 nm. In vitro experiments indicated that the micelles were unstable below pH 6.5. After encapsulation of PTX within the micelles, dynamic light scattering (DLS) studies indicated that low pH had a similar demicellization effect. An in vitro release study indicated that PTX was slowly released at pH 7.4 (normal body conditions) but rapidly released under weakly acidic conditions (pH 6.0). We demonstrated the safety of micelles from in vitro cytotoxicity tests on HeLa cells and the in vivo anti-tumor activity of PTX-PM in B16F 10 tumor-bearing mice. We concluded that these pH-sensitive micelles have potential as carriers for anti-cancer drugs.

• BMB Reports
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• v.44 no.4
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• pp.267-272
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• 2011

ZAS3 is a large zinc finger transcription repressor that binds the ${\kappa}B$-motif via two signature domains of ZASN and ZASC. A loss-of-function study showed that lack of ZAS3 protein induced accelerated cell proliferation and tumorigenesis. Conversely, gain-of-function studies showed that ZAS3 repressed $NF{\kappa}B$-activated transcription by competing with $NF{\kappa}B$ for the ${\kappa}B$-motif. Based on these observations, we hypothesize that ZAS3 promotes apoptosis by interrupting anti-apoptotic activity of $NF{\kappa}B$. Here, we present evidence that upon $TNF{\alpha}$ stimulation, ZAS3 inhibits $NF{\kappa}B$-mediated cell survival and promotes caspase-mediated apoptosis. The inhibitory effect of ZAS3 on $NF{\kappa}B$ activity is mediated by neither direct association with $NF{\kappa}B$ nor disrupting nuclear localization of $NF{\kappa}B$. Instead, ZAS3 repressed the expression of two key anti-apoptotic genes of $NF{\kappa}B$, TRAF1 and TRAF2, thereby sensitizing cells to $TNF{\alpha}$-induced cell death. Taken together, our data suggest that ZAS3 is a tumor suppressor gene and therefore serves as a novel therapeutic target for developing anti-cancer drugs.