• The Journal of Korean Obstetrics and Gynecology
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• v.18 no.1
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• pp.15-28
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• 2005

To address the ability of Kung-Kyung-Ilho-Jeon(KK) to induce cell death, we investigated the effect of KK on cell viability. Forty-eight hours later, loss of viability occurred following KK exposure in a dose-dependent manner. The treatment of KK, a commonly used herb formulation in Korea and China, caused a decrease in cell viability. KK also resulted in apoptotic morphology a brightly blue-fluorescent condensed nuclei by Hoechst 33258-staining, and reduction of cell volume. Our results show that KK induces caspase-3 and -9 activation in a time-dependent manner. In addtion, the translocation of cytochrome c release into cytoplasm has been observed under the presence of $5mg/m{\ell}$ KK. The subsequent loss of mitochondria membrane potential is collapsed by the addition of KK. Our immunoblotting data show that PARP, a well known caspase-3 and -6 substrate, is cleaved by KK. We show that a pro-apoptotic protein, Bax is increased in the presence of KK but that the amount of Bcl-2 is not changed. We suggest that Bax, a critical protein which can regulate channel of mitochondria to release cytochrome c, is a key protein in KK-induced apoptosis of Hela human cervical carcinoma cells

• Journal of Microbiology and Biotechnology
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• v.30 no.6
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• pp.885-892
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• 2020

Chemotherapy regimens for non-small cell lung cancer (NSCLC) have various adverse effects on the human body. For this reason, probiotics have received attention regarding their potential value as a safe and natural complementary strategy for cancer prevention. This study analyzed the anticancer effects of aqueous extracts of probiotic bacteria Bifidobacterium bifidum (BB), Bifidobacterium longum (BL), Bifidobacterium lactis (BLA), Bifidobacterium infantis 1 (BI1), and Bifidobacterium infantis 2 (BI2) on NSCLC cell lines. When the aqueous extracts of probiotic Bifidobacterium species were applied to the NSCLC cell lines A549, H1299, and HCC827, cell death increased considerably; in particular, the aqueous extracts from BB and BLA markedly reduced cell proliferation. p38 phosphorylation induced by BB aqueous extract increased the expression of cleaved caspase 3 and cleaved poly (ADP-ribose) polymerase (PARP), consequently inducing the apoptosis of A549 and H1299 cells. When the p38 inhibitor SB203580 was applied, phosphorylation of p38 decreased, and the expression of cleaved caspase 3 and cleaved PARP was also inhibited, resulting in a reduction of cell death. In addition, BB aqueous extracts reduced the secretion of MMP-9, leading to inhibition of cancer cell invasion. By contrast, after transfection of short hairpin RNA shMMP-9 (for a knockdown of MMP-9) into cancer cells, BB aqueous extracts treatment failed to suppress the cancer cell invasiveness. According to our results about their anticancer effects on NSCLC, probiotics consisting of Bifidobacterium species may be useful as adjunctive anticancer treatment in the future.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.677-683
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• 2003

We investigated the effects of Insamsapye-tang (ISSPT) water extract on the growth of human lung carcinoma A549 cells. Upon treatment with ISSPT extract, a concentration-dependent inhibition of cell viability was observed and cells developed many of the hallmark features of apoptosis, including condensation of chromatin. Flow cytometry analysis confirmed that ISSPT treatment increased populations of apoptotic-sub G1 phase. In addition, proteolytic degradation of poly(ADP-ribose) polymerase (PARP) and β-catenin protein were observed after treatment of ISSPT extract. These apoptotic effects of ISSPT in A549 cells were associated with marked inhibition of Bel-xL expression in a dose-dependent manner, however the levels of Bcl-2 and Bax expression were not affected. ISSPT treatment also induced the expression of tumor suppressor p53 mRNA and inhibited the expression of caspase-3 mRNA. The previous and present results indicated that ISSPT-induced inhibition of lung cancer cell proliferation is associated with the blockage of G1/S progression and the induction of apoptosis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.5
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• pp.1370-1374
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• 2005

The Tosyl-JM3 (TJM3) is a modified compound from one of 1,2,3,4-Tetra- hydroisoquinoline (THIQ) derivatives. The THIQs include potent cytotoxic agents that display a range of anti-tumor activities, antimicrobial activity, and other biological properties. In this study, we investigated the effect of TJM3 on the cytotoxicity, induction of apoptosis in human promyelocytic leukemia cells (HL-60 cells). TJM3 showed a significant cytotoxic activity in HL-60 cells (IC50 = approximately $60{\mu}g/m{\ell}$) after a 24 hr incubation. Treatment of HL-60 cells with TJM3 exhibited several features of apoptosis, including formation of DNA ladders in agarose gel electrophoresis, morphological changes of HL-60 cells with DAPI stain. Here we observed that TJM3 caused a decrease of procaspase-3 protein. Further molecular analysis demonstrated that TJM3 led to cleavage of poly(ADP-ribose) polymerase (PARP) by western blot and increase of hypodiploid (Sub-G1) population in the flow cytometric analysis. In conclusion, these above results indicate that TJM3 dramatically suppresses HL-60 cell growth and induces apoptosis. These data may support a possibility for the use of TJM3 in the prevention and treatment of leukemia.

• Korean Journal of Plant Resources
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• v.28 no.3
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• pp.297-304
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• 2015

The flower buds of Sophora japonica L (SF), as a well-known traditional Chinese medicinal herb, have been used to treat bleeding-related disorders such as hematochezia, hemorrhoidal bleeding, dysfunctional uterine bleeding, and diarrhea. However, no specific anti-cancer effect and its molecular mechanism of SF have been described. Thus, we performed in vitro study to investigate if treatment of SF affects activating transcription factor 3 (ATF3) expression and ATF3-mediated apoptosis in human colorectal cancer cells. The effects of SF on cell viability and apoptosis were measured by MTT assay and Western blot analysis against cleaved poly (ADP-ribose) polymerase (PARP). ATF3 activation induced by SF was evaluated using Western blot analysis, RT-PCR and ATF3 promoter assay. SF treatment caused decrease of cell viability and increase of apoptosis in a dose-dependent manner in HCT116 and SW480 cells. Exposure of SF activated the levels of ATF3 protein and mRNA via transcriptional regulation in HCT116 and SW480 cells. Inhibition of extracellular signal-regulated kinases (ERK) 1/2 by PD98059 and p38 by SB203580 attenuated SF-induced ATF3 expression and transcriptional activation. Ectopic ATF3 overexpression accelerated SF-induced cleavage of PARP. These findings suggest that SF-mediated apoptosis may be the result of ATF3 expression through ERK1/2 and p38-mediated transcriptional activation.

• Journal of Food Hygiene and Safety
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• v.36 no.1
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• pp.100-104
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• 2021

trans-Cinnamaldehyde (TCA), as one of the active ingredients in cinnamon, has been reported to have antiviral, antibacterial and antifungal effects as well as anti-cancer effects in several cancer cell lines. However, reports of TCA in gastric cancer are rare, and its mechanism is unclear. In this study, we investigated the anti-proliferative effect of TCA and its mechanism in gastric cancer AGS cells. TCA dose-dependently inhibited the cell viability of AGS cells. Our results suggested that TCA induces apoptosis through changes in cell morphology. To elucidate its mechanism, we investigated the expression level of apoptosis-related proteins. TCA induced the expression of p53 and Bax proteins, and then increased the cleaved caspase 9 and cleaved PARP. These results indicated that TCA triggers apoptosis via p53 pathway in AGS cells. Our results suggested that TCA might be a new anticancer drug candidate for gastric cancer.

• The Journal of Korean Obstetrics and Gynecology
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• v.22 no.1
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• pp.125-139
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• 2009

Purpose: This experiment was designed to find out increasing effects of S. barbata. co-treatment with anti-cancer drugs at cancer cell's growth inhibition effect. Methods: Divergent observational study of the S. barbata. co-treatment with Cisplatin treatment on HeLa cell. Cell viability using MTT assay, Cell Culture and Cytotoxicity Studies, Cell Cycle Analysis, Annexin V-FITC/PI assay, Cell morphological assessment, PARP cleavage using Western blotting analysis when HeLa cell were co-treated with Cisplatin and Scutellaria Barbata extracts. Results: When HeLa cell were co-treated with Cisplatin and Scutellaria Barbata extracts, we found out viability of HeLa cell, changing in the distribution of cell cycle, Annexin V-FITC staining, DAPI staining, PARP clavage protein assay by Western-blot. So Scutellaria Barbata extracts have increased apoptosis Conclusion: When co-treated Scutellaria Barbata extracts with anti-cancer drugs, the anti-cancer effects were increased. We still not sure which constituent apoptosis at cancer cells and activates anti-cancer effects suppressing, but we believe that it'll be revealed here after with following experiments.

• Journal of Life Science
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• v.21 no.12
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• pp.1678-1688
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• 2011

The apoptogenic effect of p-coumaric acid, a phenolic acid found in various edible plants, on human acute leukemia Jurkat T cells was investigated. Exposure of Jurkat T cells to p-coumaric acid (50-$150{\mu}M$) caused cytotoxicity and TdT-mediated dUTP nick-end labeling (TUNEL)-positive apoptotic DNA fragmentation along with Bak activation, ${\Delta}{\psi}m$ loss, activation of caspase-9, -3, -7, and -8, and PARP degradation in a dose-dependent manner. However,these apoptotic events were completely abrogated in Jurkat T cells overexpressing Bcl-2.Under these conditions, necrosis was not accompanied. Pretreatment of the cells with the pan-caspase inhibitor (z-VAD-fmk) could prevent p-coumaric acid-induced sub-$G_1$ peak representing apoptotic cells, whereas it failed to block ${\Delta}{\psi}m$ loss, indicating that the activation of caspase cascade was prerequisite for p-coumaric acid-induced apoptosis as a downstream event of ${\Delta}{\psi}m$ loss. FADD- and caspase-8-positive wild-type Jurkat T cell clone A3, FADD-deficient Jurkat T cell clone I2.1, and caspase-8-deficient Jurkat T cell clone I9.2 exhibited similar susceptibilities to the cytotoxicity of p-coumaric acid, excluding an involvement of Fas/FasL system in triggering the apoptosis. The apoptogenic activity of p-coumaric acid is more potent in malignant Jurkat T cells than in normal human peripheral T cells. Together, these results demonstrated that p-coumaric acid-induced apoptogenic activity in Jurkat T cellswas mediated by Bak activation, ${\Delta}{\psi}m$ loss, and subsequent activation of multiple caspases such as caspase-9, -3, -7, and-8, and PARP degradation, which could be regulated by anti-apoptotic protein Bcl-2.

• Journal of Life Science
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• v.20 no.8
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• pp.1281-1286
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• 2010

Gaucher disease (GD) is caused by glucocerebrosidase functional deficiency and the most prevalent lysosomal storage disorder (LSD), with an incidence of about 1 in 20,000 new births. Resveratrol, one kind of phytoalexin, is a produced naturally by several plants and has anti-tumor, anti-aging, anti-inflammatory and neuro-protective effects. In this paper we provide the cellular protective effect of resveratrol in both type I and type II Gaucher disease cells. Resveratrol treatment did not show any significant change in the p21 and p53 mRNA expression level, however expression level of the p21 protein, a cell cycle arrest factor, shows significant increment in both types of Gaucher disease cells. These cell cycle arrest patterns were confirmed by both MTT assay measurement and microscopy detection. In comparison, expression level of poly ADP ribose polymerase (PARP), an apoptosis indicator protein, was significantly decreased in both type I and II Gaucher disease cells after treatment with resveratrol. This result indicates that resveratrol relievescellular apoptotic stress fromtype I and II Gaucher disease cells. Therefore, we demonstrate that resveratrol inhibits cell proliferation via p21 activity and activates cellular repair systems for Gaucher disease cells. Our results provide at least one of the molecular mechanisms of Gaucher disease and may allow the verification of potential drug targets for therapeutic trials.

• Journal of Oriental Neuropsychiatry
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• v.20 no.2
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• pp.111-120
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• 2009

Objectives : This study was performed to investigate the effects of Needle Electrode Electrical Stimulation (NEES) on ischemia-induced cerebrovascular accidents. After obstruction and reperfusion of ${\ast}{\ast}$ arteries in white mice, the amounts of necrosis and inflammation related substances IL-6, Caspase-3, and PARP, C-fos were measured in neurons of the hippocampus. The following results were obtained. Methods : This study used 21 male specific pathogen free (SPF) SD (Sprague Dawley) rats, 8 weeks of age and approximately 300 g in weight, that were given at least 1 week to adapt to the lab environment Each exposed artery was completely occluded with non-absorbent suture thread and kept in that state for 5 minutes. The sutures were then removed to allow reperfusion of blood. Test group is control group for comparison with the common carotid artery occlusion models, a GI group that underwent common carotid artery occlusion, and a needle electrode electrical stimulation (NEES) group that underwent NEES after artery occlusion. The GI and NEES groups were given 12, 24, or 48 hours of reperfusion before NEES. NEES device (PG6, ITO, Japan, 9V, current, 2Hz) was used to stimulate the right and left acupoint ST36 of the SD rats for 30 minutes while they were sedated with 3% isoflurane. An immunohistochemistry test was done on the forebrains of the GI induced rats. All the data collected from this study was symbolized and analyzed using a statistics processing program (SPSS 12.0K/PC). The level of significance was set at ${\alpha}$=0.05 and a T-TEST analysis was used to find out the effects of treatment on each of the groups: the normal group, the CVA induced group, and the treatment after CVA induction group. Results : Both PARP and C-fos immuno-reactive cells, related to apoptosis, were greater in the GI groups than the NEES group. Caspase and IL-6 immuno-reactive cells, related to inflammation, were greater in the GI and NEES groups than the control group. Conclusions : This research was conducted to study the effects of NEES on CVA due to ischemia. Occlusion and reperfusion was performed on the common carotid arteries of white rats, after which amounts of substances related to neuron necrosis and inflammation - PARP, IL-6, Caspase-3, and C-fos - were measured in the Hippocampus