• 대한한방내과학회지
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• 제27권2호
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• pp.379-393
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• 2006

Objectives: We are aimed to identify anti-tumor effects of Curcuma aromatics on some kinds of cancer cells through molecular biologic methods. Materials & Methods: We used 4 kinds of cancer cell lines such as lung cancer cells(AS49), cervical cancer cells(HeLa), glioma cancer cells(A172) and prostate cancer cells(PC3). We treated the boiled extract of Curcuma aromatica $5{\mu}g,\;10{\mu}g$ to cultural media(ml) for 24 hours. We measured the cytotoxicitv on 4 kinds of cancer cells through tryphan blue exclusion test and the suppressive effect on viability of 4 kinds of cancer cells via MTT assay. We measured change of mitochondria membrane potential via flow cytometry. The quantitative RT-PCR was used to examine the effect on the revelation of Bcl-2 and Bax which are genes related to apoptosis. We examined the effect on the revelation of Bcl-2 Protein and Bar protein by western blot analysis. Results : In the experiment of tryphan blue exclusion test, the extract of Curcuma aromatica showed more significant killing effect on AS49, HeLa than the control group with density dependent manner, which was statistically significant. In the experiment of MTT assay the extract of Curcuma aromatica showed more suppressive effect on viability of A549, HeLa than the control group with density dependent manner, which was statistically significant. Curcuma aromatica induced apoptosis by decreasing the membrane potential of mitochondria in A549, HeLa. In the experiment of the revelation of genes related to apoptosis, the revelation of Bcl-2 decreased and the revelation of Bax increased in A549, HeLa treated with Curcuma aromatica with dose dependent manner. In the experiment of the revelation of protein related to apoptosis, the protein levels of Bcl-2 decreased and the protein levels of Bax increased in AS49, HeLa treated with Curcuma aromatica with dose dependent manner. Conclusions: From this study, we can infer that Curcuma aromatica has anti-tumor effect on lung cancer cells and uterine carcinoma cells but not on glioma cells and prostate cancer cells.

• Transactions on Electrical and Electronic Materials
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• 제13권3호
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• pp.157-161
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• 2012

In this study, we investigated the etching characteristics of ITO thin films and the effects of inert gases added to $Cl_2/BCl_3$ inductivity coupled plasma. The maximum etch rate of ITO thin film was 130.0 nm/min upon the addition of Ar (6 sccm) to the $Cl_2/BCl_3$ (4:16 sccm) plasma, which was higher than that with He or $N_2$ added to the plasma. The ion bombardment by $Ar^+$ sputtering was due to the relatively low volatility of the by-products formed in the $Cl_2/BCl_3$ (4:16 sccm) plasma. The surface of the etched ITO thin film was characterized by x-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). From the XPS results, it is concluded that the proper addition of Ar and He to the $Cl_2/BCl_3$ plasma removes carbon and by-products from the surface of the etched ITO thin film.

• 대한한방내과학회지
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• 제27권2호
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• pp.429-443
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• 2006

Objectives : The Purpose of this study was to identify anti-tumor effects of Curcuma longa L. on some kinds of cancer cells through molecular biologic methods. Materials & Methods : We used 4 kinds of cancer cell lines such as glioma cells(A172), cervical cancer cells(HeLa), Prostate cancer cells(PC3), lung cancer cells(A549). We injected the boiled extract of Curcuma longa L. $5{\mu}g,\;10{\mu}g$ to culture media(ml) for 24 hours. We measured the cytotoxic effect on 4 kinds of cancer cells through trypan blue exclusion test and the suppressive effect on viability of 4 kinds of cancer cells via MTT assay. We measured the change of mitochondria membrane potential via flow cytometry. The quantitative RT-PCR was used to examine the effect on the revelation of Bcl-2 and Bax which genes are related to apoptosis. We examined the effect on the revelation of Bcl-2 protein and Bax protein by western blot analysis. Results: 1. Extract of Curcuma longa L. showed significant cytotoxic effect on A172, HeLa, PC3 compared to the control group with density dependent manner. 2. Extract of Curcuma longs L. showed significant suppressive effect on viability of A172, HeLa, PC3 compared to the control group with density dependent manner. 3. Curcuma longs L. induced apoptosis by decreasing the membrane potential of mitochondria in A172, HeLa, PC3. 4. In the test about the revelation of genes related to apoptosis, the revelation of Bcl-2 decreased and the revelation of Bax increased in A172. HeLa, PC3 treated with Curcuma longa L. with density dependent manner. 5. In the test about the revelation of protein related to apoptosis, the protein levels of Bcl-2 decreased and the protein levels of Bax increased in A172, HeLa, PC3 treated with Curcuma longa L. Conclusions: This experiment shewed that Curcuma longs L. has anti-tumor effect on glioma, cervical, Prostate cancer cells except on lung cancer. We hope that anti-tumor effects of Curcuma longa L. will be more Practically identified.

• Clinical and Experimental Pediatrics
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• 제53권10호
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• pp.898-908
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• 2010

Purpose: The neuroprotective effects of erythropoietin (EPO) have been recently shown in many animal models of brain injury, including hypoxic-ischemic (HI) encephalopathy, trauma, and excitotoxicity; however, limited data are available for such effects during the neonatal periods. Therefore, we investigated whether recombinant human EPO (rHuEPO) can protect against perinatal HI brain injury via an antiapoptotic mechanism. Methods: The left carotid artery was ligated in 7-day-old Sprague-Dawley (SD) rat pups ($in$ $vivo$ model). The animals were divided into 6 groups: normoxia control (NC), normoxia sham-operated (NS), hypoxia only (H), hypoxia+vehicle (HV), hypoxia+rHuEPO before a hypoxic insult (HE-B), and hypoxia+rHuEPO after a hypoxic insult (HE-A). Embryonic cortical neuronal cell culture of SD rats at 18 days gestation ($in$ $vitro$ model) was performed. The cultured cells were divided into 5 groups: normoxia (N), hypoxia (H), and 1, 10, and 100 IU/mL rHuEPO-treated groups. Results: In the $in$ $vivo$ model, Bcl-2 expressions in the H and HV groups were lower than those in the NC and NS groups, whereas those in the HE-A and HE-B groups were greater than those of the H and HV groups. The expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were in contrast to those of Bcl-2. In the $in$ $vitro$ model, the patterns of Bcl-2, Bax, and caspase-3 expression and Bax/Bcl-2 ratio were similar to the results obtained in the in vivo model. Conclusion: rHuEPO exerts neuroprotective effect against perinatal HI brain injury via an antiapoptotic mechanism.

• 대한한방부인과학회지
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• 제18권4호
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• pp.10-23
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• 2005

Purpose : This study is to examine the ability of Rhizoma Scirpi (RS) to induce HeLa cell viability. Methods : We culture HeLa cell which is human metrocarcinoma cell in D-MEM included 10% fetal bovine serum(Hyclone Laboratories) below $37^{\circ}C$, 5% CO2. Then we observed apoptosis of log phage cell which is changed cultivation liquid 24 Hours periodically. Results : 1. RS induces mitochondria membrane potential collapse. 2. P38 MAPK is involved in RS-induced death in HeLa cells. 3. P38 MAPK is involved in RS-induced apoptosis in HeLa cells. 4. P38 MAPK reguates RS-induced caspase-3, -8 and -9 activation in HeLa cells. 5. The inhibition of caspase regulates RS-induced cell death in HeLa cells. 6. RS induces mitochondria membrane potential collapse in HeLa cells. 7. P38 MPK is involved in the regulation of Bcl-2 and Bfu in HeLa cells.8. RS regulates the expression of Bcl-2 and Bax in HeLa cells. 9. SR induces p38 MAPK activation in HeLa cells. Conclusion : RS induces apoptosis in HeLa cells via p38 MAPK activation.

• Molecules and Cells
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• 제24권3호
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• pp.378-387
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• 2007

The Bcl-2 family of proteins interacts at the mitochondria to regulate apoptosis. However, the anti-apoptotic Bcl-2 and $Bcl-X_L$ are not completely localized to the mitochondria. In an attempt to generate Bcl-2 and $Bcl-X_L$ chimeras that are constitutively localized to the mitochondria, we substituted their C-terminal transmembrane tail or both the C-terminal transmembrane tail and the adjacent loop with the equivalent regions from Bak or Bax mutant (BaxS184V) as these regions determine the mitochondrial localization of Bak and Bax. The effects of these substitutions on subcellular localization and their activities were assessed following expression in HeLa and CHO K1 cells. The substitution of the C-terminal tail or the C-terminal tail and the adjacent loop of Bcl-2 with the equivalent regions from Bak or the Bax mutant resulted in its association with the mitochondria. This change in subcellular localization of Bcl-2 chimeras triggered cells to undergo apoptotic-like cell death. The localization of this Bcl-2 chimera to the mitochondria may be associated with the disruption of mitochondrial membrane potential. Unlike Bcl-2, the loop structure adjacent to the C-terminal tail in $Bcl-X_L$ is crucial for its localization. To localize the $Bcl-X_L$ chimeras to the mitochondria, the loop structure next to the C-terminal tail in $Bcl-X_L$ protein must remain intact and cannot be substituted by the loop from Bax or Bak. The chimeric $Bcl-X_L$ with both its C-terminal tail and the loop structure replaced by the equivalent regions of Bak or Bax mutant localized throughout the entire cytosol. The $Bcl-X_L$ chimeras that are targeted to the mitochondria and the wild type $Bcl-X_L$ provided same protection against cell death under several death inducing conditions.

• Asian Pacific Journal of Cancer Prevention
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• 제14권6호
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• pp.3631-3634
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• 2013

MicroRNAs (MiRNAs) play important roles in coordinating a variety of cellular processes and abnormal expression has been linked to the occurrence of several cancers. The miRNA miR-451 is downregulated in colorectal carcinoma (CRC) cells, suggested by several research groups including our own. In this study, synthetic miR-451 mimics were transfected into the SW620 human CRC cell line using Lipofectamine 2000 and expression of miR-451 was analyzed by real time PCR, while expression of CAB39, LKB1, AMPK, AKT, PI3K and Bcl2 was analyzed by Western blot, and cell growth was detected by MTT assay. In comparison to the controls, a significant increase in the expression of miR-451 was associated with significantly decreased expression of CAB39, LKB1, AMPK, AKT, PI3K and Bcl2. The capacity of cell proliferation was significantly decreased by miR-451 expression, which also inhibited cell growth. Our study confirmed that miR-451 has a repressive role in CRC cells by inhibiting cell growth through down-regulating the P13K/AKT pathway.

• 대한한방부인과학회지
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• 제24권3호
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• pp.14-27
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• 2011

Objectives: This study was designed to investigate the effects of Acanthopanacis Cortex Radicis extract(ACRE) on the apoptosis in HeLa cell and MCF-7 cell. Methods: After treatment with various concentration of ACRE, cell growth was evaluated in HeLa cell and MCF-7 cell. Hoechst 33342 staining was performed to estimate DNA fragment effect of ACRE on the apoptosis in HeLa cell and MCF-7 cell. Annexin V/PI apoptosis assay was used to estimate the effects of ACRE on the early apoptosis in HeLa cell and MCF-7 cell. RT-PCR was used to estimate the apoptosis gene expression effect of ACRE on Hela cell MCF-7 cell. Results: Under $0.1mg/m\ell$ of ACRE, cytotoxic effect was not found per NIH3T3 cell. The viability of HeLa cell and MCF-7 cells was significantly decreased ACRE ($100{\mu}g/m\ell$) in HeLa cell and MCF-7 cell, ACRE ($50{\mu}g/m\ell$) in HeLa cell 3 days after treatment, in MCF-7 cell 1&3 days after treatment (p<0.01). DNA fragmentation was observed 3 days after treatment of cl of ACRE on HeLa cell and MCF-7 cell. In Annexin V/PI apoptosis assay, after treatment of $100{\mu}g/m\ell$ of ACRE, the early apoptotic cell increased both in HeLa cell and MCF-7 cell. In RT-PCR analysis, after treatment of $100{\mu}g/m\ell$ of ACRE, bcl-2 were decreased and bax, caspase-3 were increased both in HeLa cell and MCF-7 cell. Conclusions: ACRE appears to have considerable activity on the apoptosis in HeLa cell and MCF-7 cell.

• 생명과학회지
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• 제17권8호통권88호
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• pp.1027-1033
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• 2007

Paclitaxel이 암세포에서 세포예정사를 유발할지라도, 아직 정확한 기전은 잘 알려져 있지 않다. 이에 본 연구에서는 HeLa $S_{3}$ 자궁암세포에서의 paclitaxel이 어떠한 영향을 미치는지 알아보고자 한다. 그리하여 방법으로는 세포독성검사, apoptotic cells의 형태학적 변화(DAPI 염색 ), western blot 분석법을 사용하여 수행하였다. 본 연구의 결과로 paclitaxel은 HeLa $S_{3}$ 세포에서 세포독성을 보이며 특히 paclitaxel의 $IC_{50}$ 값은 약 1 ${\mu}M$이며, paclitaxel 처리한 HeLa $S_{3}$ 세포에서 형태학적 변화(분절화)를 관찰하였고, flow cytometric 분석에서는 G2/M기가 차단되어 paclitaxel은 세포주기 특히 Sub-$G_{1}$기를 조절함을 알 수 있다. 그리고 Paclitaxel을 처리한 HeLa $S_{3}$ 세포에서는 PARP cleavage를 유발하였고 Bc1-2의 감소와도 관련되었다.

• 한국동물학회:학술대회논문집
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• 한국동물학회 2003년도 한국생물과학협회 학술발표대회
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• pp.196.3-196
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• 2003

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