• Proceedings of the Korean Magnetic Resonance Society Conference
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• 2000.01a
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• pp.18-18
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• 2000

• Proceedings of the Korean Magnetic Resonance Society Conference
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• 2001.02a
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• pp.26-26
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• 2001

• Archives of Pharmacal Research
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• v.27 no.3
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• pp.324-333
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• 2004

To determine whether Insulin-like growth factor (IGF-I) treatment represents a potential means of enhancing the survival of cardiac muscle cells from adriamycin (ADR)-induced cell death, the present study examined the ability of IGF-I to prevent cell death. The study was performed utilising the embryonic, rat, cardiac muscle cell line, H9C2. Incubating cardiac muscle cells in the presence of adriamycin increased cell death, as determined by MTT assay and annexin V-positive cell number. The addition of 100 ng/mL IGF-I, in the presence of adriamycin, decreased apoptosis. The effect of IGF-I on phosphorylation of PI, a substrate of phosphatidylinositol 3-kinase (PI 3-kinase) or protein kinase B (AKT), was also examined in H9C2 cardiac muscle cells. IGF-I increased the phosphorylation of ERK 1 and 2 and $PKC{\;}{\zeta}{\;}kinase$. The use of inhibitors of PI 3-kinase (LY 294002), in the cell death assay, demonstrated partial abrogation of the protective effect of IGF-I. The MEK1 inhibitor-PD098059 and the PKC inhibitor-chelerythrine exhibited no effect on IGF-1-induced cell protection. In the regulatory subunit of PI3K-p85- dominant, negative plasmid-transfected cells, the IGF-1-induced protective effect was reversed. This data demonstrates that IGF-I protects cardiac muscle cells from ADR-induced cell death. Although IGF-I activates several signaling pathways that contribute to its protective effect in other cell types, only activation of PI 3-kinase contributes to this effect in H9C2 cardiac muscle cells.

• Tuberculosis and Respiratory Diseases
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• v.51 no.2
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• pp.122-134
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• 2001

Background : Some chemotherapeutic drugs induce NF-${\kappa}B$ activation by degrading the $I{\kappa}B{\alpha}$ protein in cancer cells which contributes to anticancer drug resistance. We hypothesized that inhibiting $I{\kappa}B{\alpha}$ degradation would block NF-${\kappa}B$ activation and result in increased tumor cell mortality in response to chemotherapy. Methods : The "superrepressor" form of the NF-${\kappa}B$ inhibitor was transferred by an adenoviral vector (Ad-$I{\kappa}B{\alpha}$-SR) to the human lung cancer cell lines (NCI H157 and NCI H460). With a MIT assay, the level of sensitization to cisplatin and paclitaxel were measured. To confirm the mechanism, an EMSA and Annexin V assay were performed. Results : EMSA showed that $I{\kappa}B{\alpha}$-SR effectively blocked the NF-${\kappa}B$ activation induced by cisplatin. Transduction with Ad-$I{\kappa}B{\alpha}$-SR resulted in an increased sensitivity of the lung cancer cell lines to cisplatin and paclitaxel by a factor of 2~3 in terms of $IC_{50}$. Annexin-V analysis suggests that this increment in chemosensitivity to cisplatin probably occurs through the induction of apoptosis. Conclusion : The blockade of chemotherapeutics induced NF-${\kappa}B$ activation by inducing Ad-$I{\kappa}B{\alpha}$-SR, increased apoptosis and increasing the chemosensitivity of the lung cancer cell lines tested, subsequently. Gene transfer of $I{\kappa}B{\alpha}$-SR appears to be a new therapeutic strategy of chemosensitization in lung cancer.

• The Korean Journal of Nuclear Medicine
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• v.38 no.2
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• pp.175-179
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• 2004

Molecular nuclear cardiac imaging has included Tc-99m Annexin imaging to visualize myocardial apoptosis, but is now usually associated with gene therapy and cell-based therapy. Cardiac gene therapy was not successful so far but cardiac reporter gene imaging was made possible using HSV-TK (herpes simplex virus thymidine kinase) and F-18 FHBG (fluoro-hydroxymethylbutyl guanine) or I-124 FIAU (fluoro-deoxyiodo-arabino-furanosyluracil). Gene delivery was performed by needic injection with or without catheter guidance. Tk expression did not last longer than 2 weeks in myocardium. Cell-based therapy of ischemic heart or failing heart looks promising, but biodistribution and differentiation of transplanted cells are not known. Reporter genes can be transfected to the stem/progenitor cells and cells containing these genes can be transplanted to the recipients using catheter-based purging or injection. Repeated imaging should be available and if promoter are varied to let express reporter transgenes, cellular (trans)differentiation can be studied. NIS (sodium iodide symporter) or D2R receptor genes are promising in this aspect.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.15
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• pp.6075-6080
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• 2014

Lung cancer is the leading cause of cancer-related death worldwide. Here we investigated the antitumor effect and mechanism of Zhejiang (Huzhou and Jiande) saffron against lung cancer cell lines, A549 and H446. Using high performance liquid chromatography (HPLC), the contents of crocin I and II were determined. In vitro, MTT assay and annexin-V FITC/PI staining showed cell proliferation activity and apoptosis to be changed in a dose- and time-dependent manner. The inhibition effect of Jiande saffron was the strongest. In vivo, when mice were orally administered saffron extracts at dose of 100mg/kg/d for 28 days, xenograft tumor size was reduced, and ELISA and Western blotting analysis of caspase-3, -8 and -9 exhibited stronger expression and activity than in the control. In summary, saffron from Zhejiang has significant antitumor effects in vitro and in vivo through caspase-8-caspase-9-caspase-3 mediated cell apoptosis. It thus appears to have more potential as a therapeutic agent.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.7
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• pp.3395-3403
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• 2016

Conjugated linoleic acid, a functional lipid, produced from Lactobacillus plantarum (LP-CLA), has been demonstrated to possess apoptotic activity. The anti-proliferative and apoptotic potential of LP-CLA was here evaluated in vitro using the MDA-MB-231 human breast cancer cell line as a model system. Proliferation of MDA-MB-231 cells was inhibited with increasing concentrations of LP-CLA with altered morphological features like cell detachment, rounding of cells and oligonucleosomal fragmentation of DNA. Flow cytometry confirmed the apoptotic potential of LP-CLA by ANNEXIN V/PI double staining. Furthermore, outcome results indicated that the apoptosis was mediated by downregulation of the NF-${\kappa}B$ pathway which in turn acted through proteasome degradation of $I{\kappa}B{\alpha}$, inhibition of p65 nuclear translocation, release of cytochrome-C from mitochondria and finally overexpression of Bax protein. Thus, conjugated linoleic acid, a natural product derived from probiotics, could therefore be a possible potential chemotherapeutic agent due to its apoptotic activity against estrogen receptor negative breast cancer cells.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.9 no.1
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• pp.15-37
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• 2003

Objective: We are aimed to identify anti-tumor effects of Curcuma longa L. on the stomach cancer cells through molecular biologic methods. Material & Methods: We used AGS as human stomach cancer cells obtained from American Type Culture Collection. The boiled extract of Curcuma longa L. $5{\mu}l$ (Sample I), $10{\mu}l$ (Sample II) was treated to cultural media(ml) for 0, 6, 12, 24, 48 hours. We measured the killing effect on stomach cancer cells through Trypan blue exclusion test and the suppressive effect on viability of stomach cancer cells via MTT assay. For identification of its anticancer mechanism, the revelation of Bcl-2, Bcl-XL, and Bax which are genes related to apoptosis using the quantitative RT-PCR, change of mitochondria membrane permeability and membrane potential via flow cytometry, the cycle of cell mitosis, caspase cleavage and annexin V staining were examined. Results: 1. showed significant killing effect on stomach cancer cell than the control group with a time(6 hours later) and density dependent manner, which was statistical significance. 2. Extract of Curcuma longa L. showed suppressive effect on viability of stomach cancer cells that each test groups had more suppressive effects on viability of stomach cancer cells than the control group with a time(6 hours later), which was statistical significance.(p<0.05) 3. In the test about the revelation of genes related to apoptosis, the revelation of Bcl-2 and Bcl-XL decreased with a density manner which was statistical significance. but the revelation of Bax was not changed with statistical significance. 4. Extract of Curcuma longa L. caused apoptosis by decreasing the absorbance of mitochondria with statistical significance, and also induced apoptosis by decreasing the membrane potential of mitochondria. 5. Extract of Curcuma longa L. destructed the cell cycle of cell mitosos. 6. Cell apoptosis was induced by extract of Curcuma longa L. certificated by method of caspase cleavage and annexin V staining. Conclusion: This experiment showed that Curcuma longa L. has anti-tumor effect with statistical significance. This is in vitro experiment and basic experiment on Curcuma longa L.. We hope more progressive research on Curcuma longa L. will go on and its anti-tumor effects will be more practically identified.

• Journal of Life Science
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• v.31 no.11
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• pp.969-979
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• 2021

Type 2 diabetes is a serious chronic metabolic disease, and the goal of diabetes treatment is to keep blood glucose at a normal level and prevent complications from diabetes. Hyperglycemia is a key pathologic feature of type 2 diabetes that mainly results from insulin resistance and pancreatic β-cell dysfunction. Chronic exposure of β-cells to elevated glucose concentrations induces glucotoxicity. In this study, we examined whether an 80% ethanol extract of Oxya chinensis sinuosa Mishchenko (OEE) protected INS-1 pancreatic β-cells against glucotoxicity-induced apoptosis and oxidative stress. Pretreatment with a high concentration of glucose (high glucose = 30 mM) induced glucotoxicity and apoptosis of INS-1 pancreatic β cells. Treatment with OEE significantly increased cell viability. Treatment with 0.01-0.20 mg/ml OEE dose dependently decreased intracellular reactive oxygen species, lipid peroxidation, and nitric oxide levels and increased insulin secretion in high glucose-pretreated INS-1 β cells. OEE also significantly increased the activities of antioxidant enzymes in response to high-glucose-induced oxidative stress. Moreover, OEE treatment significantly reduced the expressions of pro-apoptotic proteins, including Bax, cytochrome C, caspase-3, and caspase-9, and increased anti-apoptotic Bcl-2 expression. Apoptotic cells were identified using Annexin-V/propidium iodide staining, which revealed that treatment with OEE significantly reduced high-glucose-induced apoptosis. These findings implicate OEE as a valuable functional food in protecting pancreatic β-cells against glucotoxicity-induced apoptosis and oxidative stress.

• Journal of Life Science
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• v.34 no.1
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• pp.9-17
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• 2024

Diabetes mellitus (DM) is one of the main global health problems. Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, a process that is termed glucose toxicity. Our perspective about glucose toxicity as it pertains to the pancreatic β-cell is that the characteristic decreases in insulin secretion are caused by regulated apoptotic gene expression. In this study, we examined whether ferulic acid protects INS-1 pancreatic cells against high glucose-induced apoptosis. High glucose concentration (30 mM) induced glucotoxicity and death of INS-1 pancreatic β cells. However, treatment with 1, 5, 10, or 20 μM ferulic acid increased the cell viability in a concentration-dependent manner. Treatment with ferulic acid dose-dependently decreased the intracellular levels of reactive oxygen species, thiobarbituric acid reactive substances, and nitric oxide in INS-1 pancreatic β cells pretreated with high glucose. These effects influence the apoptotic pathway, increasing the expression of the anti-apoptotic protein Bcl-2 and reducing the levels of pro-apoptotic proteins, including Bax, cytochrome C, and caspase 9. Annexin V/propidium iodide staining indicated that ferulic acid significantly reduced high glucose-induced apoptosis. These results demonstrate that ferulic acid is a potential therapeutic agent to protect INS-1 pancreatic β cells against high glucose-induced apoptosis.