• Journal of Physiology & Pathology in Korean Medicine
• /
• v.23 no.6
• /
• pp.1349-1357
• /
• 2009

This study was performed to investigate the effects of Shigyungbanha-tang(SGT) on the lipopolysaccharide(LPS) induced acute lung injury(ALI) in mice. 1 and 24 h before LPS intratracheal instillation, control group was taken distilled water orally. Treated groups was taken each concentrate SGT(2.5 g/kg, 6.7 g/kg) by orally as same times. Normal group was not instilled with LPS and was taken distilled water. 24 h after LPS intratracheal instillation, lung histology was performed in inflated-fixed lungs in 3 mice of each groups. The other mice of each groups, bronchoalveolar lavege fluids(BALF) was obtained to measure proinflammatory cytokines(TNF-$\alpha$, IL-$1{\beta}$, IL-6) and blood sample was obtained to measure white blood cell(WBC). In vitro, the effect of SGT($100\;ug/m{\ell}$, $500\;ug/m{\ell}$, $1000\;ug/m{\ell}$) on the release of RANTES, TARC induced by TNF-$\alpha$ and IL-4 in human alveolar epithelial cell(A549) was examined. Histopathologically, SGT prevented LPS-induced lung injury. SGT decreased protein, TNF-$\alpha$, IL-$1{\beta}$ and IL-6 according to concentrations. In vitro, $500\;ug/m{\ell}$, $1000\;ug/m{\ell}$ concentrate SGT suppressed the expression of RANTES and TARC on A549 cells. On the basis of these results, SGT had a markedly anti-inflammatory effect in a clinically relevant model of ALI. Nevertheless, further investigations are required to determine the potential clinical usefulness of SGT in the adjunctive therapy of ALI.

• KSBB Journal
• /
• v.14 no.1
• /
• pp.9-16
• /
• 1999

Transforming growth factor $\beta$1(TGF-$\beta$1) has potentials to be used as a new therapeutic agent. However, studies with TGF-$\beta$ were hindered by its high cost. In this study, we developed an improved method to purify TGF-$\beta$1 from human platelets, for which four purification steps were used: platelet extraction, gel filtration, cation exchange chromatography, and reverse phase high performance liquid chromatography. After a final step of purification, a pure protein with a molecular weight of 25,000 corresponding to the commercially available TGF-$\beta$1 was obtained, which were confirmed by silver staining and Western blotting after SDS-polyacrylamide gel electrophoresis (SDS-PAGE). It was confirmed by the inhibitory effects of TGF-$\beta$1 on a mink lung epithelial cell line that the purified TGF-$\beta$1 had its biological activity, whose activity is slightly higher than that of the commercially available TGF-$\beta$1. About 3.7$\mug of the purified TGF-$\beta$1 was obtained from 10 units of concentrated human platelets, the final yield of which is about 21%.

• Journal of Life Science
• /
• v.17 no.11
• /
• pp.1596-1600
• /
• 2007

Bee venom is used to treat inflammatory diseases in Korean traditional medicine and has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in bee venom-induced apoptosis are still uncharacterized in human lung cancer cells. In the present study, we investigated the effects of bee venom on the apoptosis of A549 human lung epithelial cancer cells. Treatment of bee venom inhibited the cell viability and induced apoptosis in a concentration-dependent manner as measured by hemocytometer counts, fluorescence microscopy and flow cytometry analysis. Bee venom-induced apoptosis in A549 cells was associated with a marked inhibition of anti-apoptotic Bcl-2 expression without significant changes in the levels of Bax and Bcl-xL. Bee venom treatment also inhibited the levels of IAP family members such as cIAP-1 and cIAP-2 and induced the proteolytic activation of caspase-3 and caspase-9. Although further studies are needed, the present results suggest that apoptotic signals evoked by bee vemon in A549 cancer cells may converge caspases activation through a down-regulation of Bcl-2 rather than an up-regulation of Bax. These findings provide important insights into the possible molecular mechanisms of the anti-cancer activity of bee vemon in human cancer cells.

• The Journal of Advanced Prosthodontics
• /
• v.7 no.2
• /
• pp.138-145
• /
• 2015

PURPOSE. The objective of this study was to conduct an in vitro comparative evaluation of polished and laser-dimpled titanium (Ti) surfaces to determine whether either surface has an advantage in promoting the attachment of epithelial-like cells and fibroblast to Ti. MATERIALS AND METHODS. Forty-eight coin-shaped samples of commercially pure, grade 4 Ti plates were used in this study. These discs were cleaned to a surface roughness (Ra: roughness centerline average) of 180 nm by polishing and were divided into three groups: SM (n=16) had no dimples and served as the control, SM15 (n=16) had $5-{\mu}m$ dimples at $10-{\mu}m$ intervals, and SM30 (n=16) had $5-{\mu}m$ dimples at $25-{\mu}m$ intervals in a $2{\times}4mm^2$ area at the center of the disc. Human gingival squamous cell carcinoma cells (YD-38) and human lung fibroblasts (MRC-5) were cultured and used in cell proliferation assays, adhesion assays, immunofluorescent staining of adhesion proteins, and morphological analysis by SEM. The data were analyzed statistically to determine the significance of differences. RESULTS. The adhesion strength of epithelial cells was higher on Ti surfaces with $5-{\mu}m$ laser dimples than on polished Ti surfaces, while the adhesion of fibroblasts was not significantly changed by laser treatment of implant surfaces. However, epithelial cells and fibroblasts around the laser dimples appeared larger and showed increased expression of adhesion proteins. CONCLUSION. These findings demonstrate that laser dimpling may contribute to improving the peri-implant soft tissue barrier. This study provided helpful information for developing the transmucosal surface of the abutment.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.12
• /
• pp.4995-5000
• /
• 2014

Background: Cancer constitutes a key pressure on public health regardless of the economy state in different countries. As a kind of highly malignant epithelial tumor, lacrimal gland adenoid cystic carcinoma can occur in any part of the body, such as salivary gland, submandibular gland, trachea, lung, breast, skin and lacrimal gland. Chemotherapy is one of the key treatment techniques, but drug resistance, especially MDR, seriously blunts its effects. As an element of the 60S large ribosomal subunit, the ribosomal protein L39-L gene appears to be documented specifically in the human testis and many human cancer samples of different origins. Materials and Methods: Total RNA of cultured drug-resistant and susceptible lacrimal gland adenoid cystic carcinoma cells was seperated, and real time quantitative RT-PCR were used to reveal transcription differences between amycin resistant and susceptible strains of lacrimal gland adenoid cystic carcinoma cells. Viability assays were used to present the amycin resistance difference in a RPL39-L transfected lacrimal gland adenoid cystic carcinoma cell line as compared to control vector and null-transfected lacrimal gland adenoid cystic carcinoma cell lines. Results: The ribosomal protein L39-L transcription level was 6.5-fold higher in the drug-resistant human lacrimal gland adenoid cystic carcinoma cell line than in the susceptible cell line by quantitative RT-PCR analysis. The ribosomal protein L39-L transfected cells revealed enhanced drug resistance compared to plasmid vector-transfected or null-transfected cells as determined by methyl tritiated thymidine (3H-TdR) incorporation. Conclusions: The ribosomal protein L39-L gene could possibly have influence on the drug resistance mechanism of lacrimal gland adenoid cystic carcinoma cells.

• Asian Pacific Journal of Cancer Prevention
• /
• v.13 no.6
• /
• pp.2429-2435
• /
• 2012

Methyl isocyanate may have a role in cancer etiology, although the link is unclear. There is evidence in the literature that it can induce cancer in animals but the carcinogenic potency is weak. Pheochromocytoma of adrenal medulla and acinar cell tumors of pancreas have been observed in methyl isocyanate exposed animals. Conversely, emerging data from population-based epidemiological studies are contradictory since there is no evidence of such cancers in methyl isocyanate exposed humans. Recently, we reported a high prevalence of breast and lung cancers in such a population in Bhopal. In vitro findings appearing in the latest scientific literature suggest that genomic instability is caused by methyl isocyanate analogs in lung, colon, kidney, ovary epithelial cells, and that hepatocytes may undergo oncogenic transformation, have obvious implications. The conflicting information prompted us to present this update over the last three decades on methyl isocyanate-induced cancers after an extensive literature search using PubMed. While the pertinent literature remains limited, with a scarcity of strong laboratory analyses and field-epidemiological investigations, our succinct review of animal and human epidemiological data including in vitro evidences, should hopefully provide more insight to researchers, toxicologists, and public health professionals concerned with validation of the carcinogenicity of methyl isocyanate in humans.

• Korean Journal of Food Science and Technology
• /
• v.53 no.2
• /
• pp.165-173
• /
• 2021

One of the major sources of air pollution is urban particulate matter (UPM), which causes lung diseases involving oxidative stress, inflammation, and cancer. Codonopsis lanceolata (CL) has been used in East Asia as a traditional oriental medicinal ingredient for lung diseases (e.g., asthma and bronchitis). However, the connection between the impact of CL and UPM in the lungs has rarely been investigated. This study aimed to confirm the inhibitory activity of the ethanol extract of CL (ECL) against oxidative stress and disruption of tight cell junctions in human pulmonary epithelial cells after exposure to UPM. As the lung cells were pre-treated with ECL, the UPM-induced increase in cellular reactive oxygen species production suppressed tight junction proteins (e.g., N-cadherin, fibronectin, occludin, zonula occludens-1, and claudin-4). These results suggest that ECL prevents the possible effects of UPM toxicity on the lungs.

• Journal of Life Science
• /
• v.32 no.4
• /
• pp.310-317
• /
• 2022

Recently, interest in the harmful factors of particulate matter (PM), a major component of air pollution, has been increasing. In particular, PM_2.5 with a diameter of less than 2.5 ㎛ is well known to induce oxidative stress accompanied by autophagy in human lung epithelial cells. However, studies on whether PM_2.5 increases autophagy under oxidative stress and whether this process is reactive oxygen species (ROS)-dependent are insufficient. Therefore, in this study, we investigated whether PM_2.5 promotes autophagy through the generation of ROS in human alveolar epithelial A594 cells. According to our results, cells co-treated with PM_2.5 and hydrogen peroxide (H₂O₂) showed a lower cell viability than cells treated with each alone, which was associated with increased total and mitochondrial ROS production. The co-treatment of PM_2.5 and H₂O₂ also increased autophagy induction, which was confirmed through Cyto-ID staining, and the expression of autophagy biomarker proteins increased. However, when ROS generation was artificially blocked by N-acetyl-L-cysteine pretreatment, the reduction in cell viability and induction of autophagy by PM_2.5 and H₂O₂ co-treatment were markedly attenuated. Therefore, the present results suggest that PM_2.5-induced ROS generation may play a critical role in autophagy induction in A549 cells.

• BMB Reports
• /
• v.52 no.12
• /
• pp.706-711
• /
• 2019

Cisplatin (Cis-DDP) is one of the most widely used anti-cancer drugs. It is applicable to many types of cancer, including lung, bladder, and breast cancer. However, its use is now limited because of drug resistance. p90 ribosomal S6 kinase (p90RSK) is one of the downstream effectors in the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) pathway and high expression of p90RSK is observed in human breast cancer tissues. Therefore, we investigated the role of p90RSK in the Cis-DDP resistance-related signaling pathway and epithelial-mesenchymal transition (EMT) in breast cancer cells. First, we discovered that MDA-MB-231 cells exhibited more Cis-DDP resistance than other breast cancer cells, including MCF-7 and BT549 cells. Cis-DDP increased p90RSK activation, whereas the inactivation of p90RSK using a small interfering RNA (siRNA) or dominant-negative kinase mutant plasmid overexpression significantly reduced Cis-DDP-induced cell proliferation and migration via the inhibition of matrix metallopeptidase (MMP)2 and MMP9 in MDA-MB-231 cells. In addition, p90RSK activation was involved in EMT via the upregulation of mRNA expression, including that of Snail, Twist, ZEB1, N-cadherin, and vimentin. We also investigated NF-κB, the upstream regulator of EMT markers, and discovered that Cis-DDP treatment led to NF-κB translocation in the nucleus as well as its promoter activity. Our results suggest that targeting p90RSK would be a good strategy to increase Cis-DDP sensitivity in triple-negative breast cancers.

• Molecules and Cells
• /
• v.41 no.3
• /
• pp.224-233
• /
• 2018

Primary cilia are solitary, non-motile, axonemal microtubule-based antenna-like organelles that project from the plasma membrane of most mammalian cells and are implicated in transducing hedgehog signals during development. It was recently proposed that aberrant SHH signaling may be implicated in the progression of idiopathic pulmonary fibrosis (IPF). However, the distribution and role of primary cilia in IPF remains unclear. Here, we clearly observed the primary cilia in alveolar epithelial cells, fibroblasts, and endothelial cells of human normal lung tissue. Then, we investigated the distribution of primary cilia in human IPF tissue samples using immunofluorescence. Tissues from six IPF cases showed an increase in the number of primary cilia in alveolar cells and fibroblasts. In addition, we observed an increase in ciliogenesis related genes such as IFT20 and IFT88 in IPF. Since major components of the SHH signaling pathway are known to be localized in primary cilia, we quantified the mRNA expression of the SHH signaling components using qRT-PCR in both IPF and control lung. mRNA levels of SHH, the coreceptor SMO, and the transcription factors GLI1 and GLI2 were upregulated in IPF compared with control. Furthermore, the nuclear localization of GLI1 was observed mainly in alveolar epithelia and fibroblasts. In addition, we showed that defective KIF3A-mediated ciliary loss in human type II alveolar epithelial cell lines leads to disruption of SHH signaling. These results indicate that a significant increase in the number of primary cilia in IPF contributes to the upregulation of SHH signals.