• Applied Microscopy
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• v.26 no.3
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• pp.315-328
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• 1996

This study aims to demonstrate the effect of SOD (superoxide dismutase), one of the antioxidant enzymes, on the ultrastructural changes in the parietal cells caused by the administration of cisplatin in the rat. A total of 60 healthy Sprague-Dawley rats weighing about 200 gm were used as experimental animals. Cisplatin (6 mg/kg) was administered intraperitoneally to rats pretreated with 15,000 unit/kg of SOD or rats without the pretreatment. The experimental animals were sacrificed at 6 hours, 12 hours, 24 hours and 3 days after the administration of cisplatin. The results were as follows: 1. SOD alone did not affect the ultrastructural changes in the gastric parietal cells in the rat. 2. Irregular shaped mitochondria, mitochondria with dim cristae, dilated cristae, ruptured outer membrane, electron lucent matrix and degenerative mitochondria were seen in cisplatin treated rat. Whorled membranous body, many lysosomes and large vacuole were observed in the gastric parietal cells in cisplatin treated rat. 3. Mitochondria with dilated cristae and electron lucent matrix and irregular shaped mitochondria were observed in the gastric parietal cells of the cisplatin treated rat with pretreatment of SOD. These results suggest that SOD attenuates the toxic effect of the cisplatin in the gastric parietal cells of the rat.

• Journal of Society of Preventive Korean Medicine
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• v.15 no.3
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• pp.127-140
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• 2011

Objectives : The research was conducted to confirm the effect of Acanthopanax senticosus harms(ASH) on the anti-tumor activities in AGS human gastric cancer cells. Methods : To examine the potential anti-tumor effect of ASH, we performed many experiments. After processing AGS cancer cells with varying concentrations 80% ethanol ASH extract, analyses by MTT, flow cytometer(FACS) and western blot were used. Results : AGS cancer cells showed decreased cell proliferation and increased contents of S phase when treated with ASH. Moreover, the Western blot experiment showed that ASH affected S phase cell cycle-related molecules(Cyclin A, p21 and p16) in AGS cells. ASH also inhibited EGFR-STAT3 pathway in AGS human gastric cancer cells. Conclusion : Based on these results, we observed that ASH arrested the cell cycle at S phase and inhibited the phosphorylation of EGFR and STAT3 proteins which reduce the cell cycle and the manifestation of the genes that are related to inhibiting cell growth in AGS cells. It can be concluded that ASH can be used in developing medicine for gastric cancer.

• Journal of Sasang Constitutional Medicine
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• v.14 no.1
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• pp.100-111
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• 2002

1. The Purpose of study An experimental study has done to examine the effect of defense on gastric mucosal damage of Jowesungcheong-tang. 2. The Material and Method of study Mice had intragastric injected with JST extract before indome thacin treatment which induces hemorrh age erosion artificially. General morphology, infiltrative cell in mucosa, the distribution of UEA-I, COX-1, MAC-1. ICAM, and Apoptotic cell were objected (Ahhreviation) JST :Jowesungcheong-tang, UEA-I : ulex europaeus agglutinin-I, COX-1: cyclooxyhenase-1, ICAM : intercellular adhesion molecule-1, GPE : Gastropathy elicitated mice 3. The results and Conclusions of study 1) The degree of hemorrhage erosion in GPE-group had increased conspicuously in gastric gland proper. JST -group were the same as normal 2) The noticeable increase of granular lecocytes and lymphocytes in GEP-group were seen, but in JST group, the configuration is decreased 3) The decrease of UEA-I positive reacted cells, COX-1, surface epithelial cells and the increase of MAC-l positive cells, ICAM-l positive cells had shown in GPE-group, but in JST-group UEA-I positive cells, COX-1 surface epithelial cells were in creased and MAC-1 positive cells, ICAM-l positive cells were decreased than GPE-group. 4) A number of apoptotic cells were distributed in hemorrhage erosion. The remarkable decrease of apoptotic cells were shown in JST-group.

• IMMUNE NETWORK
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• v.4 no.4
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• pp.244-249
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• 2004

Background: Corticotropin-Releasing Hormone (CRH), an important regulator of stress response, has a potent immunoregulatory effect with the ability to promote the growth of various cancer through CRH receptor type 1 under stress. Although the metastasized cancers through cell migration are more aggressive than the primary cancers, little is known about the effect of CRH on cell migration. Gastric cancer is prone to metastasize to other tissues and it is reported that gastric cancer is response to various stresses such as oxidative stress. Herein, we studied the relationship between CRH and gastric cancer cell migration. Methods: We used gastric cancer cell line, MKN-28 and tested the CRH receptor type 1 expression on MKN-28 by RT-PCR. To examine the change in the ability of migration by CRH in MKN-28, cells were incubated with CRH and then migration ability was measured using a cell migration assay. Results: We confirmed that CRH receptor type 1 was expressed in MKN-28 and HaCaT cells. The migration ability of MKN-28 cells was increased by CRH in a time-, dose- dependent manner. Conclusion: These data suggest that CRH increases migration ability in gastric cancer cell line and that CRH may be a critical regulator in the metastasis of gastric cancer cell.

• The Journal of Korean Medicine
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• v.24 no.2
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• pp.94-108
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• 2003

Objectives : This study was carried out to investigate the anti-ulcer effects of Pyeongwibunsoeum extract and Misoprostol on indomethacin-induced gastric mucosal lesions of mice. Methods : Experimental groups were classified into non-treated group, non-administered group, Misoprostol-administered group and Pyeongwibunsoeum-extract-administered group. This study examined the morphological change, distribution of mast cells and apoptic cells, PNA reaction, COX-1, BrdU, NF-B p50, COX-2, IL-2R-, and ICAM-1of gastric mucosa. Results : 1. The hemorrhagic erosion of gastric mucosa was reduced in the Misoprostol-administered and Pyeongwibunsoeum-extract-administered groups. 2. The Misoprostol-administered group and Pyeongwibunsoeum-extract-administered group showed positive reaction on the PNA distribution. 3. The distribution of apoptic cells, activity of NF-B p50, COX-2, IL-2R-, and ICAM-1 decreased in both the Misoprostol-administered group and Pyeongwibunsoeum-extract-administered group. 4. The Misoprostol-administered and Pyeongwibunsoeum-extract-administered groups showed increase on COX-1, BrdU. Conclusions : As the results indicate, hemorrhagic erosion of gastric mucosa were reduced in both the Misoprostol-administeredand Pyeongwibunsoeum-extract-administered groups, and severe inflammatory reaction of gastric mucosa was reduced. The effects on the Pyeongwibunsoeum-extract-administered group were superior to those on the Misoprostol-administered group. Pyeongwibunsoeum extract can be widely administered for gastric ulcer disease in clinical treatments.

• Journal of Pharmacopuncture
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• v.16 no.3
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• pp.39-45
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• 2013

Objectives: Buxus Microphylla var. Koreana Nakai Extract (BMKNE) is used as a folk remedy for malaria and veneral disease. In the present study, we investigated the effects of BMKNE in the growth and the survival of AGS cells, the most common human gastric adenocarcinoma cell lines. Methods: The AGS cells were treated with varying concentrations of BMKNE. Analyses of the sub G1 peak, the caspase-3 and -9 activities, and the mitochondrial depolarization were conducted to determine whether AGS cell death occured by apoptosis. Also, to identify the role of transient receptor potential melastatin (TRPM) 7 channels in AGS cell growth and survival, we used human embryonic kidney (HEK) 293 cells overexpressed with TRPM7 channels. Results: Experimental results showed that the sub G1 peak, the caspase-3 and -9 activities, and the mitochondrial depolarization were increased. Therefore, BMKNE was found to induce the apoptosis of these cells, and this apoptosis was inhibited by SB203580 (a p38 mitogen-activated protein kinase (MAPK) inhibitor), and by a c-jun NH2-terminal kinase (JNK) II inhibitor. Furthermore, BMKNE inhibited TRPM7 currents and TRPM7 channel over-expressions in HEK 293 cells, exacerbating BMKNE-induced cell death. Conclusions: These findings indicate that BMKNE inhibits the growth and the survival of gastric cancer cells due to a blockade of the TRPM7 channel's activity and MAPK signaling. Therefore, BMKNE is a potential drug for treatment of gastric cancer, and both the TRPM7 channel and MAPK signaling may play an important role in survival in gastric cancer cells.

• Journal of Ginseng Research
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• v.37 no.2
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• pp.201-209
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• 2013

Ginsenoside, one of the active ingredients of Panax ginseng, has a variety of physiologic and pharmacologic effects. The purpose of this study was to explore the effects of ginsenoside Rd (G-Rd) on melastatin type transient receptor potential 7 (TRPM7) channels with respect to the proliferation and survival of AGS and MCF-7 cells (a gastric and a breast cancer cell line, respectively). AGS and MCF-7 cells were treated with different concentrations of G-Rd, and caspase-3 activities, mitochondrial depolarizations, and sub-G1 fractions were analyzed to determine if cell death occurred by apoptosis. In addition, human embryonic kidney (HEK) 293 cells overexpressing TRPM7 channels were used to confirm the role of TRPM7 channels. G-Rd inhibited the proliferation and survival of AGS and MCF-7 cells and enhanced caspase-3 activity, mitochondrial depolarization, and sub-G1 populations. In addition, G-Rd inhibited TRPM7-like currents in AGS and MCF-7 cells and in TRPM7 channel overexpressing HEK 293 cells, as determined by whole cell voltage-clamp recordings. Furthermore, TRPM7 overexpression in HEK 293 cells promoted G-Rd induced cell death. These findings suggest that G-Rd inhibits the proliferation and survival of gastric and breast cancer cells by inhibiting TRPM7 channel activity.

• IMMUNE NETWORK
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• v.11 no.1
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• pp.50-58
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• 2011

Background: Epstein-Barr virus associated gastric lymphoepithelioma-like carcinoma (LELC) is characterized by the intensive infiltration of lymphoid cells, the presence of EBV, and the better prognosis over typical adenocarcinoma. Thus, it was assumable that viral latent proteins may be responsible for the recruitment of a certain T cell repertoire to EBV-associated gastric carcinoma. Methods: To examine above possibility, EBV gene expression in gastric carcinoma tissues and usage of TCR among the tumor infiltrating lymphocytes were analyzed. Results: EBV specific DNA and EBERs RNA were detected in 4 out of 30 patients. RT-PCR analysis revealed that all 4 of EBV-positive tumor tissues expressed EBNA1 mRNA and BARTs and LMP2a was detected only one sample out of 4. However, the EBNA2 and LMP-1 transcripts were not detected in these tissues. $CD8^+$ T cells were the predominant population of infiltrating lymphocytes in the EBV-positive gastric carcinoma. According to spectra type analysis of infiltrating T cells, 10 predominant bands were detected by TCR $V{\beta}$ CDR3 specific RT-PCR from 4 EBV-positive tumor tissues. Sequence analysis of these bands revealed oligoclonal expansion of T cells. Conclusion: These findings suggest that clonally expanded T cells in vivo might be a population of cytotoxic T cells reactive to EBV-associated gastric carcinoma.

• The Journal of Internal Korean Medicine
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• v.19 no.2
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• pp.185-207
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• 1998

In order to study the immunohistochemical effects of Opae-san on gastric ulcer induced by HCl-aspirin in rats, experiments were done by oral administration and measure histological features of ulcer lesion, scaning electron microscopic appearance, the changes of numbers of parietal cells, chief cells, gastrin and somatostatin-immunoreactive cells. The obtained results are as follows: 1. Ulcerative lesions were numerously detected in control groups especially in junction of cardiac-fundic gastric mucosa and histologically very severe injury to gastric epithelium were observed too but in the Opae-san administrated groups, no gross lesion of ulcer were detected and histologically minor injury of gastric mucosa were observed. Most slight injuries to gastric mucosa were observed in 5 days after treatment. 2. The numbers of parietal cells were remarkably increased in control group but in Opae-san administrated groups appeared significant decrease compared to control groups. Most remarkably decrease of the numbers of parietal cells compared to control groups were observed in 5 days after treatment. 3. The numbers of chief cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably increase of the numbers of chief cells compared to control groups were observed in 5 days after treatment. 4. The numbers of gastrin-immunoreactive cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably decrease of the numbers of gastrin-immunoreactive cells compared to control groups were observed in 5 days after treatment. 5. The numbers of somatostatin-immunoreactive cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably decrease of the numbers of somatostatin-immunoreactive cells compared to control groups were observed in 5 days after treatment. 6. Scaning electron microscopically, severe denude and degeneration of gastric mucosa were observed in control groups but in Opae-san administrated groups the lesions were remarkably decreased compared to control groups.

• BMB Reports
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• v.50 no.8
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• pp.411-416
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• 2017

The endoplasmic reticulum (ER) membrane protein complex subunit 6 (EMC6) is a novel human autophagy-related molecule. Here, using tissue microarray and immunohistochemistry, we report that EMC6 protein is lost or reduced in glandular cells of patients with gastric adenocarcinoma, compared to normal stomach mucosa. Overexpression of EMC6 in gastric cancer cells inhibited cell growth, migration, invasion, and induced apoptosis and cell cycle arrest at S-phase. Further investigation suggested that EMC6 overexpression in BGC823 human adenocarcinoma gastric cancer cells reduced tumorigenicity in a xenograft model, demonstrating that EMC6 has the characteristics of a tumor suppressor. This is the first study to show that EMC6 induces cell death in gastric cancer cells. The molecular mechanism of how EMC6 functions as a tumor suppressor needs to be further explored.