• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.1
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• pp.93-97
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• 2007

We previously reported the anti-proliferative effect of Chungjogupae-tang (CJGPT) in human lung carcinoma A549 cells, which was associated with the induction of cyclin-dependent kinase inhibitor p21 in a tumor suppressor p53-independent manner. CJGPT treatment also resulted in the inhibition of prostaglandin E2 release A549 cells by the down-regulation of cyclooxygenase-2. In the present study, we investigated the pathway of the induction of apoptotic cell death by CJGPT in A549 cells. It was found that CJGPT could inhibit the cell viability and induce the apoptotic cell death of A549 cells in a dose-dependent manner as measured by hemocytometer counts, flow cytometry analysis and agarose gel electrophoresis. Apoptosis of A549 cells by CJGPT was associated with a down-regulation of anti-apoptotic Bcl-2 and inhibitor of apoptosis proteins (IAPs) expression. Additionally, DNA fragmentation by CJGPT was connected with the activation of inhibitor of caspase-activated DNase/DNA fragmentation factor 45 (ICAD/DFF45) protein expression.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.6
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• pp.1441-1447
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• 2003

The purpose of this research was to investigate the effects of Chungjokupye-tang(CJKPT) on the anti-carcinogenic action. The cell viability of mouse spienocytes and thymocytes were enhanced by the addition of CJKPT. CJKPT were increased of splenic and thymic T lymphocytes, such as T/sub H/ cells were markedly increased by the treatment of CJKPT in vivo. CJKPT treatment induced the apoptotic cell death of Jurkat and HL60 leukemia cells. CJKPT reduced mitochondrial transmembrane potential and increased the expression of ICE, c-myc and p53 gene in Molt-4cells dose dependant manner. These results suggest that CJKPT have an anti-carcinogenic action via immunoregulatory mechanism.

• Journal of Physiology & Pathology in Korean Medicine
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• v.29 no.2
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• pp.174-179
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• 2015

Transcription factor, Nrf2 was well known to protect cell from oxidative stress by up-regulating it's dependent anti-oxidative genes such as HO-1 and NQO1. Cheongjogupye-tang (CJGPT), a traditional herbal formula was originally recorded in 『EuiMunBeopRyul』, still having been used to treat pulmonary disease such as asthma and pulmonary inflammation, in Eastern Asian countries. However, the underlying therapeutic mechanisms remain elusive. The purpose of this study is to investigate the anti-inflammatory or anti-oxidative effects of CJGPT on the RAW 264.7 cells. To examine the anti-inflammatory or anti-oxidative effects of CJGPT, MTT assay, immunoblotting, RT-PCR and reporter gene assays were performed. Although CJGPT slightly suppressed the nuclear NF-κB expression, it did not decreased the expression of pro-inflammatory genes in LPS-stimulated RAW 264.7 cells. Moreover, it did not increased the transcriptional activity of NF-κB in reporter gene assay. However, CJGPT upregulated the nuclear expression of Nrf2, as well as increased the expression of Nrf2-dependent genes such as HO-1 and NQO1. In addition, CJGPT incresed the transcriptional activity of Nrf2. Taken together, our results showed that CJGPT exerts functions as an anti-oxidant mainly by activating Nrf2.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.19 no.2
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• pp.26-39
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• 2006

Objective : The effect of water extract of Chungjogupae-tang (CJGPT) was investigated on the growth of human lung carcinoma A549 cells. Methods : MTT assay and fluorescent microscope performed to compare and examine the efficacy of CJGPT treatment on the cytostaticity of lung cancer cells in proportion to time and doses, and DAPI staining and Western blot analysis were used to examine their effect on apoptosis. In addition the quantitative RT-PCR was used to examine to lung cancer cells growth and Progtaglandin E2 and Telomerase activity were measured Results : Exposure of A549 cells to CJGPT resulted in the growth inhibition and apoptosis in a dose-dependent manner as measured by MTT assay and fluorescent microscope. The antiuoliferative effect by CJGPT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CJGPT treatment resulted in an up-regulation of cyclin-dependent kinase inhibitor p21(WAF1/CIPl) in a p53-independent fashion. We found that CJGPT treatment decreased the levels of cyclooxygenase (COX)-2 and inducible nitric oxide synthease (iNOS) expression without significant changes in the expression of COX-1, which was correlated with a decrease in protaglandin E2 (PGE2) synthesis. CJGPT treatment also inhibited the levels of human telomerase reverse transcriptase (hTERT) and telomerase-associated protein (TEP)-1 mRNA expression, however the activity of telomerase was slightly increased by CJGPT treatment. Conclusion : These findings suggested that CJGPT-induced inhibition of human lung carcinoma A549 cell growth was connected with the induction of apoptotic cell death and the results provided important new insights into the possible molecular mechanisms of the anti-cancer activity of CJGPT.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.4
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• pp.966-972
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• 2006

The effect of water extract of Chungjogupae-tang (CJGPT) was investigated _on the growth of human lung carcinoma A549 cells. Methods: MTT assay and fluorescent microscope peformed to compare and examine the efficacy of CJGPT treatment on the cytostaticity of lung cancer cells in proportion to time and doses, and DAPI staining and Western blot analysis were used to examine their effect on apoptosis. In addition, the quantitative RT-PCR was used to examine to lung cancer cells growth, and Prostaglandin E2 activity were measured. Results: Exposure of A549 cells to CJGPT respited in the growth inhibition and apoptosis in a dose-dependent manner as measured by MTT assay and fluorescent microscope. The antiproliferative effect by CJGPT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CJGPT treatment resulted in an up-regulation of cyclin-dependent kinase inhibitor p21 (WAFl/CIPl) in a p53-independent fashion. We found that CJGPT treatment decreased the levels of cyclooxygenase (COX)-2 and inducible nitric oxide synthease (iNOS) expression without significant changes in the expression of COX-1 , which was correlated with a decrease in prostaglandin E2 (PGE2) synthesis. Conclusion: These findings suggested that CJGPT-induced inhibition of human lung carcinoma A549 cell growth was connected with the induction of apoptotic cell death and the results provided important new insights into the possible molecular mechanisms of the anti-cancer activity of CJGPT.

• The Journal of Internal Korean Medicine
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• v.29 no.2
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• pp.318-333
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• 2008

Objectives : In this study, the author tried to examine whether Cheogjogupye-tang (淸燥救肺湯, CGPT) and Yieum-jeon (理陰煎, YEJ) significantly affect in vitro and in vivo mucin secretion, MUC5AC gene expression in airway epithelial cells and contractility of isolated tracheal smooth muscle of rabbit. Materials and Methods : For in vitro experiment, confluent hamster tracheal surface epithelial (HTSE) cells were chased for 30 minutes in the presence of CGPT and YEJ to assess the effects of the agents on mucin secretion by enzyme-linked immunosorbent assay (ELISA), with removal of oriental herbal medicine extract from each agent-treated sample by centrifuge microfilter. Also, the effects of the agents on TNF-alpha or EGF-induced MUC5AC gene expression in human airway epithelial cells (NCI-H292) were investigated. Possible cytotoxicities of the agent were assessed by examining both LDH release from HTSE cells and the rate of survival and proliferation of NCI-H292 cells. For in vivo experiment, hypersecretion of airway mucin and goblet cell hyperplasia was induced by exposure of rats to $SO_2$ over 3 weeks. Effects of CGPT and YEJ orally administered for 1 week on in vivo mucin secretion from tracheal goblet cells of rats and hyperplasia of goblet cells were assessed using ELISA and histological analysis after staining the epithelial tissue with alcian blue, respectively. Also, the effects of CGPT and YEJ on contractility of isolated tracheal smooth muscle were investigated. Results : (1) CGPT significantly inhibited in vitro mucin secretion from cultured HTSE cells. However, YEJ did not affect in vitro mucin secretion; (2) CGPT and YEJ did not affect hypersecretion of in vivo mucin and hyperplasia of tracheal goblet cells; (3) CGPT and YEJ slightly increased the expression levels of TNF-alpha or EGF-induced MUC5AC gene in NCI-H292 cells; (4) CGPT and YEJ inhibited acetylcholine-induced contraction of isolated tracheal smooth muscle of rabbit; (5) CGPT and YEJ did not affect LDH release from HTSE cells and the survival and proliferation of NCI-H292 cells. Conclusion : The results from the present study suggest that CGPT and YEJ mainly affect the expression of mucin gene rather than secretion of mucin and do not show remarkable cytotoxicity to respiratory epithelial cells.