• The Korean Journal of Physiology and Pharmacology
• /
• v.21 no.3
• /
• pp.327-334
• /
• 2017

Epidemiologic interest in particulate matter (PM) is growing particularly because of its impact of respiratory health. It has been elucidated that PM evoked inflammatory signal in pulmonary epithelia. However, it has not been established $Ca^{2+}$ signaling mechanisms involved in acute PM-derived signaling in pulmonary fibroblasts. In the present study, we explored dust particles PM modulated intracellular $Ca^{2+}$ signaling and sought to provide a therapeutic strategy by antagonizing PM-induced intracellular $Ca^{2+}$ signaling in human lung fibroblasts MRC5 cells. We demonstrated that PM10, less than $10{\mu}m$, induced intracellular $Ca^{2+}$ signaling, which was mediated by extracellular $Ca^{2+}$. The PM10-mediated intracellular $Ca^{2+}$ signaling was attenuated by antioxidants, phospholipase blockers, polyADPR polymerase 1 inhibitor, and transient receptor potential melastatin 2 (TRPM2) inhibitors. In addition, PM-mediated increases in reactive oxygen species were attenuated by TRPM2 blockers, clotrimazole (CLZ) and N-(p-amylcinnamoyl) anthranilic acid (ACA). Our results showed that PM10 enhanced reactive oxygen species signal by measuring DCF fluorescence and the DCF signal attenuated by both TRPM2 blockers CLZ and ACA. Here, we suggest functional inhibition of TRPM2 channels as a potential therapeutic strategy for modulation of dust particle-mediated signaling and oxidative stress accompanying lung diseases.

• 대한예방의학회:학술대회논문집
• /
• 1995.10a
• /
• pp.247-248
• /
• 1995

• Proceedings of the Korea Society of Environmental Toocicology Conference
• /
• 1996.12a
• /
• pp.69-69
• /
• 1996

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.17 no.6
• /
• pp.1479-1486
• /
• 2003

In order to evaluate the antiallergic effects of Kamiohihyosan(KCHS), studies were done. We measured the cytotoxic activity for lung fibroblast cell, cytokines transcript expression, production of IL-4, IL-10, IFN-γ, proliferation of B cell in anti-CD40mAb plus rIL-4 stimulated murine splenic B cells. The results were obtained as follows: KCHS was not showed cytotoxicity in the fibroblast lung cell, KCHS increased the gene synthesis of INF-γ, TNF-α, IL1-β, IL-6, IL-10(m-RNA), KCHS decreased the gene synthesis of IL-4, IL-5, TGF-β(m-RNA), KCHS decreased the appearance of IL-4, IgE significantly, KCHS increased the appearance of IL-10, IFN-γ significantly, KCHS decreased the proliferation of B cell significantly, The facts above prove that KCHS is effective against the allergy. Thus, I think that we should study on this continuously.

• Journal of Korean Society of Occupational and Environmental Hygiene
• /
• v.24 no.2
• /
• pp.160-168
• /
• 2014

Objectives: Chemical hazard evaluations are important for workers' health and working environments. Allyl chloride (CAS No. 107-05-1) is used in many industries, leading to concerns about the possibility of threats to the health of workers. Since only insufficient or controversial information is available about potential related hazards, an in vitro mammalian chromosomal aberration (CA) assay was conducted in order to gain additional information concerning any such hazards. Moreover, toxicological information from this study could be applied for workers' rights to know, and to prepare or update the Materials Safety Data Sheet (MSDS) for a number of industries. Methods and Results: The assay was performed using the Chinese hamster lung fibroblast cell (ATCC, CRL-1935), by the direct method (-S9) and by the metabolic activated method (+S9 mix). Using the direct method, the seven dosages in the 48-hour treatment group did not show that the frequency of CA is proportionate to the dosage. The frequency of CA is not proportionate to the dosage addition for a six-hour treatment using the metabolic activated method. Conclusions: From these findings, it was decided that this chemical does not induce chromosomal aberrations under the tested conditions.

• Korean Journal of Pharmacognosy
• /
• v.36 no.1 s.140
• /
• pp.34-37
• /
• 2005

Reactive oxygen species (ROS) are known to cause oxidative modification of DNA, proteins, lipids and small cellular molecules and are associated with tissue damage and are the contributing factors for inflammation, aging, cancer, arteriosclerosis, hypertension and diabetes. We screened the anti-oxidants in V79-4 hamster lung fibroblast cells induced by hydrogen peroxide with eighteen pure compounds isolated from natural products. Allantoin, brassicasterol, and hypaconitine were found to strongly scavenge intracellular reactive oxygen species, which is measured by dichlorodihydrofluorescin diacetate method (DCHF-DA), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical.

• Natural Product Sciences
• /
• v.13 no.2
• /
• pp.118-122
• /
• 2007

We have studied the cytoprotective effect on H$_2$O$_2$ induced oxidative stress from leaves of Carpinus tschonoskii. The methanol extract of Carpinus tschonoskii was found to scavenge intracellular reactive oxygen species (ROS) using flow cytometry and confocal microscope. This extract prevented lipid peroxidation and thus reduced cell death of Chinese hamster lung fibroblast (V79-4) induced by H$_2$O$_2$ treatment. The extract increased catalase activity and phosphorylation of extracellular signal regulated kinase (ERK). Taken together, the results suggest that Carpinus tschonoskii protects V79-4 cells against oxidative damage by H$_2$O$_2$ through scavenging ROS.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.17 no.4
• /
• pp.1065-1074
• /
• 2003

In order to evaluate the antiallergic effects of Kamiyukgunja-tang (KYGJT), studies were done. We measured the cytotoxic activity for lung fibroblast cell, cytokines transcript expression, production of INF-γ, IL-10, IL-4, GM-CSF, IL-1 β, TNF-α. IL-5 proliferation of B cell in anti-CD40mAb plus r1L-4 stimulated murine splenic B cells. The results were obtained as follows : 1. KYGJT was not showed cytotoxicity in the fibroblast lung cell. 2. KYGJT increased the gene synthesis of INF-γ, IL-10, GM-CSF(m-RNA). 3. KYGJT decreased the gene synthesis of IL-1β, IL-4, TNF-α, IL-5(m-RNA). 4. KYGJT decreased the appearance of TNF-α significantly. 5. KYGJT decreased the appearance of IgE significantly. 6. KYGJT decreased the proliferation of B cell significantly. 7. KYGJT decreased the appearance of Histamin Release Production significantly. The facts above prove that KYGJT is effective against the allergy. Thus. I think that we should study on this continuously

• Clinical and Experimental Pediatrics
• /
• v.51 no.8
• /
• pp.879-885
• /
• 2008

Purpose : The human lung fibroblast may act as an immunomodulatory cell by providing pro-inflammatory cytokines and chemokines, which are important in airway remodeling. Vascular endothelial growth factor (VEGF) induces mucosal edema and angiogenesis. Thymus and activation regulated chemokine (TARC) induces selective migration of T helper 2 cells. We investigated whether human lung fibroblasts produced VEGF and TARC, and the effects were augmented with the co-culture of fibroblasts and human bronchial smooth muscle cells (HBSMC), and whether dexamethasone can inhibit the proliferation and the release of VEGF in lung fibroblasts. Methods : Human lung fibroblasts were cultured with and without HBSMC, growth-arrested in serum-deprived medium, and pretreated with dexamethasone for 16 hours. After 24-hour stimulation with platelet derived growth factor-BB (PDGF-BB) and/or transforming growth factor-${\beta}$ (TGF-${\beta}$), culture supernatant was harvested for assays of VEGF and TARC. Cell proliferation was assayed using BrdU cell proliferation ELISA kit. Results : 1) The release of VEGF was significantly increased after stimulation with TGF-${\beta}$, and its release was augmented when co-stimulated with PDGF and TGF-${\beta}$. 2) VEGF release induced by PDGF or TGF-${\beta}$ was inhibited by dexamethasone. 3) There was no synergistic effect on the release of VEGF when human lung fibroblasts were co-cultured with HBSMC. 4) Dexamethasone did not suppress human lung fibroblasts proliferations. 5) Neither TGF-${\beta}$ nor PDGF induced TARC release from lung fibroblasts. Conclusion : Human lung fibroblasts may modulate airway remodeling by release of VEGF, but they have no synergistic effects when co-cultured with HBSMC. Dexamethasone suppresses VEGF release, not proliferation of lung fibroblast.

• Toxicological Research
• /
• v.18 no.2
• /
• pp.159-165
• /
• 2002

Recently, we reported (korean J. Biomed. Lab. Sci., 6(4): 245-251, 2000) that cyclohexane (l.56 g/kg of body wt., i.p.) administration led to lung injury in rats. However the detailed mechanism remain to be elucidated. This study was designed to clarify the mechanism of lung damage induced by cyclohexane in rats. First, lung damage was assessed by quantifying bronchoalveolar lavage fluid (BAL) protein content as well us by histopathological examination. Second, activities of serum xanthine oxidase (XO), pulmonary XO and oxygen free radical scavenging enzymes. XO tope conversion (O/D + O, %) ratio and content of reduced glutathione (GSH) were determined. In the histopathological findings, the vasodilation, local edema and hemorrhage were demonstrated in alveoli of lung. And vascular lumens filled with lipid droplets, increased macrophages in luminal margin and increased fibroblast-like interstitial cells in interstitial space were observed in electron micrographs. The introperitoneal treatment of cyclohexane dramatically increased BAL protein by 21-fold compared with control. Cyclohexane administration to rats led to a significant rise of serum and pulmonary XO activities and O/D + O ratio by 47%,30% and 24%, respectively, compared witれ control. Furthermore, activities of pulmonary oxygen free radical scavenging enzymes such as superoxide dismutase, glutathione peroxidase and glutathione S-transferase, and GSH content were not found to be statistically different between control and cyclohexane-treated rats. These results indicate that intraperitoneal injection of cyclohexane to rats may induce the lipid embolism in pulmonary blood vessel and lead to the hypoxia with the ensuing of oxygen free radical generation, and which may be responsible for the pulmonary injury.