• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2005년도 생물공학의 동향(XVI)
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• pp.210-213
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• 2005

본 연구에서는 세포 사멸을 억제시켜 재조합 단백질의 생산을 향상시키기 위한 전략을 개발하기 위해, 우선 STR-G와 EGCG를 농도별로 첨가하여 세포 성장, 사멸 그리고 IDS 생산성에 미치는 영향을 조사하였다. Flow cytometry 분석 결과, STR-G에 의한 apoptotic cell percentage의 감소, STR-G와 EGCG에 의한 bel-2 expression level의 증가와 IDS 생산성의 증가를 확인하였다.

• 동의생리병리학회지
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• 제21권4호
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• pp.992-997
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• 2007

Cisplatin is a chemotherapeutic drug which is widely used for cancer therapy including cervical cancer. The purpose of this study is to elucidate synergistic effect of Cisplatin and Berberine on the apoptosis of HeLa cells and to determine whether oxidants are formed as part of apoptotic process. Apoptotic death of HeLa cells by cisplatin and berberine was confirmed by chromatin condensation of HeLa cells and flow cytometric analysis of intracellular ROS(reactive oxygen species) production. In MTT assay, Cell viability was decreased and enhanced ROS generation in combination of cisplatin and berberine significantly, as compared with cisplatin only. Synergistic effect of Cisplatin and Berberine on the inhibition of cell growth by apoptosis was clearly observed and ROS may play an important role in apoptosis. This effect suggest the possibility lowering the concentration of chemotherapeutic drugs, which alleviate the side effect of drugs.

• 생명과학회지
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• 제29권12호
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• pp.1393-1400
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• 2019

본 연구에서는 사람의 제대정맥 내피세포에서 고농도 당에 의해 유도되는 세포사멸과 연관된 미토콘드리아의 기능적 지표 변화에 미치는 diazoxide의 효과를 관찰하였다. 고농도 당에 노출된 내피세포에서 세포사멸이 시간에 따라 증가하였고, caspase 3와 8, 9의 활성 증가가 동반되었다. Caspase 3와 9의 억제제들이 세포사멸을 감소시킨 반면 caspase 8의 억제제는 효과가 없었다. 고농도 당에 노출된 세포에서 미토콘드리아 막전위의 탈분극과 막투과도의 증가, 치토크롬 C (cytochrome C)의 유리가 동반됨을 관찰할 수 있었다. Diazoxide는 고농도 당에 의한 미토콘드리아 의존성 세포사멸 신호의 활성화를 억제하였다. Diazoxide의 이러한 효과들은 미토콘드리아막의 ATP-억제성 칼륨통로 차단제인 5-hydroxydecanoate에 의해 차단되었다. 이상의 결과들을 종합하면 diazoxide가 미토콘드리아막의 ATP-억제성 칼륨통로 개방을 통해 미토콘드리아 의존성 세포사멸 신호기작의 활성화를 차단하여 고농도 당에 의해 유도되는 세포사멸을 억제하는 것으로 사료된다.

• 대한소아치과학회지
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• 제24권3호
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• pp.688-703
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• 1997

The effect of glossopharyngeal nerve transection on the taste buds of the rat vallate papilla was examined by using the method of DNA nick-end labeling (TUNEL) and standard electron microscopic technique at 1, 3, 5, 7, 9 days after denervation. In general, the number and size of taste buds decreased as more days passed after denervation. They started decreasing on day 3 post denervation and virtually all taste buds were disappeared on day 9 post denervation. In studies using TUNEL method, TUNEL postive cells markedly increased in their numbers one day post denervation, as compared with controls. The number of apoptotic taste bud cells per taste bud profile was averaged to be 0.64 and 0.44 for day 1 and 3 post denervation, respectively, whereas it was 0.10 in controls. In electron microscopy, apoptotic cells were identified by the presence of condensed and fragmentary nuclei in a cytoplasm, which resulted in increased density. In control rats, only few apoptotic cells were found. On days 1 and 3 post denervation, nerve fibers almost disappeared from the taste buds and some apoptotic cells were apparent. On days 7 and 9 post denervation, a few taste bud cells were still present in the epithelium of the bottom of the trench wall of the vallate papilla and most of them showed apoptotic changes. The results indicate that the death of taste bud cells in normal conditions is controlled by apoptosis and the decrease and disappearance of taste buds after denervation is also caused by apoptosis of taste bud cells.

• Journal of Acupuncture Research
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• 제20권3호
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• pp.45-62
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• 2003

Objective : To examine the effects of Beevenom on the cell proliferation of human breast carcinoma cell line MCF-7, we performed various experiments such as does-dependent effect of Beevenom on cell proliferation and viability, morphological changes, and alterations of apoptosis/cell cycle-regulatory gene products. Methods : Beevenom induced cell viability and proliferation of MCF-7 cells in a concentration-dependent manner. The anti-proliferative effect by Beevenom treatment in MCF-7 cells was associated with morphological changes such as membrance shrinking and cell rounding up. Results : Beevenom induced apoptotic cell death in a concentration-dependent manager, which was associated with degradation of ${\beta}$-catenin, an apoptotic target protein. Beevenom induced the Bax expressions, a pro-apoptotic gene, both in protein and mRNA levels, however, the levels of Bcl-$X_{S/L}$ expression, an anti-apoptotic gene, were down-regulated in Beevenom-treated cells. Western blot analysis and RT-PCT data revealed that the levels of cyclin of B1 protein and cyclin E mRNA were reduced by Beevenom treatment in MCF-7 cells, respectively, where as the expression of tumor suppressor p53 and cyclin dependent kinase inhibitor p21 mRNA were markedly increased in a concentration-dependent fashion. Conclusions : Taken together, these findings suggest that Beevenom induced inhibition of human breast cancer cell proliferation is associated with the induction of apoptotic cell death and Beevenom may have therapeutic potential in human breast cancer.

• 대한방사선치료학회지
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• 제12권1호
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• pp.166-173
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• 2000

Angiopoietin-1(Ang-1) is a vasculogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. We examined the effect of angiopoietin-1(Ang-1) on radiation-induced apoptosis in human umbilical vein endothelial cells(HUVECS) and receptor/second messenger signal transduction pathway for Ang-1's effect on HUVECs. The percent of apoptotic cells under control condition(0Gy) was $8.2\%$. Irradiation induced apoptosis was increased in a dose(1, 5, 10, and 15Gy)- and time 12, 24, 48 and 72hr)-dependent manner. The percent of apoptotic cells was approximately $34.9\%$ after 15 Gy of irradiation. Under these conditions, pretreatment with Ang-1's (50, 100, 200, and 400 ng/ml) inhibited irradiation-induced apoptosis in human umbilical vein endothelial cells in a dose-dependent manner. Two hundred ng/ml of Ang-1 inhibited approximately $55-60\%$ of the apoptotic events that occurred in the 10 Gy-irradiated cells. Pre-treatment with soluble Tie2 receptor, but not Tie1 receptor, blocked the Ang-1's antiapoptotic effects. Phosphatidylinositol 3'-kinase (P13-kinase) specific inhibitor, wortmanin and LY294002, blocked the Ang-1-induced antiapoptotic effect. Ang-1 promotes the survival of endothelial cells in irradiation-induced apoptosis through Tie2 receptor binding and P13-kinase activation. Pretreatment of Ang-1 could be beneficial in maintaining normal endothelial cell integrity during irradiation therapy.

• International Journal of Industrial Entomology and Biomaterials
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• 제27권2호
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• pp.228-236
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• 2013

Breast cancer is one of the most common cancers among women worldwide. Recently anticancer agents have been developed using natural substances. To evaluate the anticancer effect of hydrolysates of silk fibroin (HSF), we investigated the effect of HSF on cell viability and apoptosis of a breast cancer cell line, MCF-7, induced through the mitochondrial pathway. The result showed that HSF decreased cell viability in MCF-7 cells in a dose- and time-dependent manner, resulting in an increase in the sub-G1 phase cell population. HSF increased the level of the pro-apoptotic Bax protein and decreased the levels of the anti-apoptotic Bcl-2 protein. In addition, HSF induced apoptosis in MCF-7 cells through a mitochondria-dependent pathway by increasing levels of cytochtome c, and cleavage of PARP. Taken together, these findings suggest that HSF inhibits the proliferation of MCF-7 breast cancer cells through a mitochondria and caspase dependent apoptotic pathway.

• Molecules and Cells
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• 제21권1호
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• pp.7-20
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• 2006

The major event in human immunodeficiency virus type 1 (HIV-1) infection is the death of many cells related to host immune response. The demise of these cells is normally explained by cell suicide mechanism, apoptosis. Interestingly, the decrease in the number of immune cells, such as non-CD4+ cells as well as CD4+ T cells, in HIV infection usually occurs in uninfected bystander cells, not in directly infected cells. It has, therefore, been suggested that several soluble factors, including viral protein R (Vpr), are released from the infected cells and induce the death of bystander cells. Some studies show that Vpr interacts directly with adenine nucleotide translocator (ANT) to induce mitochondrial membrane permeabilization (MMP). The MMP results in release of some apoptogenic factors such as cytochrome-c (cyt-c) and apoptosis-inducing factor (AIF). Vpr also has indirect effect on mitochondria through enhancing the level of caspase-9 transcription and suppressing nuclear factor-kappa B (NF-${\kappa}B$). The involvement of p53 in Vpr-induced apoptosis remains to be studied. On the other hand, low level of Vpr expression has anti-apoptotic effect, whereas it's high level of expression induces apoptosis. Extracellular Vpr also exhibits cytotoxicity to uninfected bystander cells through apoptotic or necrotic mechanism. The facts that Vpr has cytotoxic effect on both infected cells and bystander cells, and that it exhibits both proand anti-apoptotic activity may explain its role in viral survival and disease progression.

• 대한의생명과학회지
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• 제24권2호
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• pp.134-137
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• 2018

S100A8 and S100A9 are involved in pathogenesis of cancer by induction or inhibition of cancer as well as inflammation. In this study, we investigated the association of S100A8 and S100A9 with pathogenesis of leukemia using human monocytic leukemia cells, THP-1. The expression of TLR4, which is a known receptor of S100A8 and S100A9, was examined by using flow cytometry and Western blotting. THP-1 cells have high surface and cytosol expression of TLR4. S100A8 and S100A9 suppressed the cell survival, and this suppression was found to be associated with apoptosis because they increased the number of apoptotic cells in a dose- and a time-dependent manners. However, S100A8 and S100A9 had no effect on the survival and apoptosis of monocytes isolated from the peripheral blood. We next examined the apoptotic effect of lipopolysaccharide (LPS) and monophosphoryl lipid A (MPLA), which are other ligands of TLR4, in THP-1 cells. Lipopolysaccharide had no effect on cell survival, but MPLA is effective on the cell apoptosis. These results suggest that S100A8 and S100A9 may regulate leukemia cell survival via TLR4, which is an essential receptor in the pro-apoptotic mechanism induced by S100A8 and S100A9. These findings may shed light on development of a possible therapeutic drug for leukemia treatment.

• 대한한의학회지
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• 제39권1호
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• pp.35-43
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• 2018

Objectives: In the brain, glutamate is the most important excitable neurotransmitter in physiological and pathological conditions. However, the high level of glutamate induces neuronal cell death due to exitotoxicity and oxidative stress. The present study investigated to evaluate a possible neuroprotective effect of furosin isolated from Euphorbia helioscopia against glutamate-induced HT22 cell death. Methods: Furosin was isolated from methanol extract of Euphorbia helioscopia and examined whether it protects glutamate-induced neuronal cell death. The cell viability was determined using Ez-Cytox assay. Anti-oxidative effect of furosin was determined by DPPH scavenging activities, and the levels of intracellular reactive oxygen species (ROS) were determined by the fluorescent intensity after staining the cells with $H_2DCFDA$. To evaluate apoptotic cell death, we performed nuclear staining and image-based cytometeric analysis. Results: The cell viability was significantly increased by treatement with furosin compared with the treatment with glutamate. Furosin showed a strong DPPH radical scavenging activity ($EC50=1.83{\mu}M$) and prevented the accumulation of intra cellular ROS. Finally, the presence of 50 and $100{\mu}M$ furosin significantly the percentage of apoptotic cells compared with glutamate treatment. Conclusion: The present study found that furosin is a potent neuroprotectant against glutamate-induced oxidative stress through inhibition of apoptotic cell death induced by glutamate. Therefore, the present study suggests that furosin as a bioactive compound of E. helioscopia can be a useful source to develop a drug for the treatment of neurodegenerative diseases and acute brain injuries.