• 동의생리병리학회지
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• 제24권6호
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• pp.1042-1052
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• 2010

This study aimed to evaluate the protective effects of Mundongcheongpye-eum (MCE) on elastase-induced lung injury. The extract of MCE was treated to A549 cells and elastase-induced lung injury mice model. Then, various parameters such as cell-based cyto-protective activity and histopathological finding were analyzed. MCE showed a protective effect on elastase-induced cytotoxicity in A549 cells. This effect was correlated with analysis for caspase 3 levels, collagen and elastin contents, protein level of cyclin B1, Cdc2, and Erk1/2, and gene expression of TNF-${\alpha}$ and IL-$1{\beta}$ in A549 cells. MCE treatment also revealed the protective effect on elastase-induced lung injury in mice model. This effect was evidenced via histopathological finding including immunofluence stains against elastin, collagen, caspase 3, and protein level of cyclin B1, Cdc2, and Erk1/2 in lung tissue. These data suggest that MCE has a pharmaceutical properties on lung injury. This study would provide an scientific evidence for the efficacy of MCE for clinical application to patients with chronic obstructive pulmonary disease.

• Journal of Microbiology and Biotechnology
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• 제33권1호
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• pp.43-50
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• 2023

Fungal keratitis is a refractory kind of keratopathy. We attempted to investigate the antiinflammatory role of thymol on Aspergillus fumigatus (A. fumigatus) keratitis. Wound healing and fluorescein staining of the cornea were applied to verify thymol's safety. Mice models of A. fumigatus keratitis underwent subconjunctival injection of thymol. The anti-inflammatory roles of thymol were verified by hematoxylin-eosin (HE) staining, slit lamp observation, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting. In contrast with the DMSO group, more transparent corneas and less inflammatory cells infiltration were detected in mice treated with 50 ㎍/ml thymol. Thymol downregulated the synthesis of TLR4, MyD88, NF-kB, IL-1β, NLRP3, caspase 1, caspase 8, GSDMD, RIPK3 and MLKL. In summary, we proved that thymol played a protective part in A. fumigatus keratitis by cutting down inflammatory cells aggregation, downregulating the TLR4/ MyD88/ NF-kB/ IL-1β signal expression and reducing necroptosis and pyroptosis.

• Toxicological Research
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• 제16권2호
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• pp.133-139
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• 2000

This study was designed to evaluate the mechanism by which reactive nitrogen intermediates (RNI) induced the cytotoxicity of human doparminergic neuroblastoma SH-SY5Y cells. 3-Morpholino-sydnonimine (SIN-l), a donor of peroxynitrite (ONOO) and sodium nitroprusside (SNP), a donor of nitric oxide (NO) induced cell detachment and apoptotic death, as characterized by chromatin condensation, the ladder pattern fragmentation of genomic DNA and morphological nuclear changes. SIN-l also induced the activation of caspase 3-like protease in a time-dependent manner. Exogenous antioxidants, such as reduced glutathione (GSH), N-acetylcysteine (NAC), and selenium protected the cells from apoptotic death and reduced the activation of caspase 3-like protease by SIN-1. Furthermore, SIN-l directly reduced the intracellular levels of glutathione. Taken together, these data suggested that RNI including NO and peroxynitrite decrease the concentration of intracellular antioxidant such as GSH, which lead to the apoptotic death of human neuroblastoma SH-SY5Y cells.

• Asian Pacific Journal of Cancer Prevention
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• 제16권16호
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• pp.7261-7266
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• 2015

Breast cancer, the most common cancer in the women, is the leading cause of death. Necrotic signaling pathways will enable targeted therapeutic agents to eliminate apoptosis-resistant cancer cells. In the present study, the effect of shikonin on the induction of cell necroptosis or apoptosis was evaluated using the T-47D breast cancer cell line. The cell death modes, caspase-3 and 8 activities and the levels of reactive oxygen species (ROS) were assessed. Cell death mainly occurred through necroptosis. In the presence of Nec-1, caspase-3 mediated apoptosis was apparent in the shikonin treated cells. Shikonin stimulates ROS generation in the mitochondria of T-47D cells, which causes necroptosis or apoptosis. Induction of necroptosis, as a backup-programmed cell death pathway via ROS stimulation, offers a new strategy for the treatment of breast cancer.

• Journal of Ginseng Research
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• 제44권3호
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• pp.373-385
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• 2020

Inflammation is an immune response that protects against pathogens and cellular stress. The hallmark of inflammatory responses is inflammasome activation in response to various stimuli. This subsequently activates downstream effectors, that is, inflammatory caspases such as caspase-1, 4, 5, 11, and 12. Extensive efforts have been made on developing effective and safe anti-inflammatory therapeutics, and ginseng has long been traditionally used as efficacious and safe herbal medicine in treating various inflammatory and inflammation-mediated diseases. Many studies have successfully shown that ginseng plays an anti-inflammatory role by inhibiting inflammasomes and inflammasome-activated inflammatory caspases. This review discusses the regulatory roles of ginseng on inflammatory caspases in inflammatory responses and also suggests new research areas on the anti-inflammatory function of ginseng, which provides a novel insight into the development of ginseng as an effective and safe anti-inflammatory herbal medicine.

• BMB Reports
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• 제42권11호
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• pp.713-718
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• 2009

Apoptotic DNA fragmentation, the hallmark of apoptosis, is mediated primarily by caspase-activated DFF40 (CAD) nuclease. DFF40 exists as a heterodimer with DFF45 (ICAD), which is a specific chaperone and inhibitor of DFF40 under normal conditions. To understand the mechanism through which the DFF40/DFF45 system is regulated, we analyzed the structural and biochemical properties of apoptotic DNA fragmentation mediated by DFF40/DFF45. Using limited proteolysis, we show that residues 1-281 of DFF45 form a rigid, crystallized domain, whereas the loop formed by residues 277-281 is accessible by trypsin. These results show that the C-terminal helix formed by residues 281-300 is dynamic and necessary for the chaperone activity of DFF45, but not for inhibition of DFF40.

• 대한의생명과학회지
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• 제26권3호
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• pp.226-229
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• 2020

S100A8 functions as an essential factor in inflammatory response. Cytokine release of monocytes and regulation of neutrophil apoptosis are important steps in pathogenesis of allergy. This study aims to examine the relation between cytokine release of monocytes due to S100A8 and neutrophil apoptosis. S100A8 enhanced the release of IL-6 and IL-8 in monocytes of normal and allergic subjects. Treatment of supernatants of normal and allergic monocytes with S100A8 blocked neutrophil apoptosis by inhibition of caspase 9 and caspase 3 activation. The secretion signal induced by S100A8 is involved in TLR4, Src family protein, PKCδ, ERK1/2, p38 MAPK, JNK, and NF-κB. These findings may contribute to understanding the complex pathogenesis of allergic diseases by determining inflammatory responses associated with S100A8, monocytes, and neutrophils.

• Archives of Pharmacal Research
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• 제29권5호
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• pp.363-368
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• 2006

EGCG [(-)-epigallocatechin-3-gallate], a major component of green tea has been considered as a major antioxidant constituent. In addition to having been considered for cancer treatment as a chemopreventive and chemotherapeutic agent, EGCG has recently been attributed an anti-proliferative effect. We re-examined the latter finding in this study and added specific focus on the ability of EGCG to induce apoptosis in human osteogenic sarcoma (HOS) cells. Antiproliferative action of EGCG $(IC_{50}=35.3{\pm}6.0{\mu}g/mL)$ appeared to be linked to apoptotic cell death based on morphological changes, chromosomal DNA degradation, and an increase in the $sub-G_1$ apoptotic cell population. Treatment of HOS cells with EGCG gradually activated caspase-3, an established inducer of apoptotic cell death.

• 대한임상검사과학회지
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• 제42권1호
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• pp.46-54
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• 2010

Ceramide induces cell death in a variety of cell types however, the underlying molecular mechanisms related to renal epithelial cells remain unclear. The present study was undertaken to determine the role of extracellular signal-regulated protein kinase (ERK) in ceramide-induced cell death in renal epithelial cells. An established renal proximal tubular cell line of opossum kidney (OK) cells was used for this research. Ceramide induced apoptotic cell death in these cells. Western blot analysis showed that ceramide induced activation of ERK. The ERK activation and cell death induced by ceramide were prevented by the ERK inhibitor PD98059. Ceramide caused cytochrome C release from mitochondria into the cytosol as well as activation of caspase-3. Both effects were prevented by PD98059. The ceramide-induced cell death was also prevented by a caspase inhibitor. These results suggest that ceramide induces cell death through an ERK-dependent mitochondrial apoptotic pathway in OK cells.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.146-146
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• 2003

20-O-(${\beta}$-D-Glucopyranosyl)-20(S)-protopanaxadiol (IH901), an intestinal bacterial metabolite of ginseng saponins formed from ginsenosides Rb1, Rb2 and Rc, is suggested to be a potential chemopreventive agent. Here we show that IH901 induces apoptosis in human hepatoblastoma HepG2 cells.(omitted)