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Tabebuia avellanedae에서 유래된 ${\beta}>-lapachone$의 인체폐암세포 apoptosis 유발에 관한 연구
최병태,이용태,최영현,Choi, Byung-Tae,Lee, Yong-Tae,Choi, Yung-Hyun 대한동의생리학회 2005 동의생리병리학회지 Vol.19 No.3
The DNA topoismerase I inhibitor ${\beta}-lapachone$, the product of a lapacho tree (Tabebuia avellanedae) from South America, activates a novel apoptotic response in a number of cell lines. In the present report, we investigated the effects of ${\beta}-lapachone$ on the growth of human lung in human non-small-cell-lung-cancer A549 cells. Upon treatment with ${\beta}-lapachone$, a concentration-dependent inhibition of cell viability and cell proliferation was observed as measured by hemocytometer counts and MTT assay. The ${\beta}-lapachone-treated$ cells developed many of the hallmark features of apoptosis, including membrane shrinking, condensation of chromatin and DNA fragmentation. These apoptotic effects of ${\beta}-lapachone$ in A549 cells were associated with a marked induction of pro-apoptotic Bax expression, however the levels of anti-apoptotic Bcl-2 expression were decreased in a dose-dependent manner. Accordingly, elevated amount of cyclin-dependent kinase inhibitor p21 expression accompanied by up-regulation of tumor suppressor p53 was observed. By RT-PCR analyses, decrease in gene expression level of telomerase reverse transcriptase and telomeric repeat binding factor were also observed. Thus, these findings suggest that ${\beta}-lapachone$ may be a potential anti-cancer therapeutics for the control of human lung cancer cell model.
Regulation of Cyclin D3 by Calpain Protease in Human Breast Carcinoma MDA-MB-231 Cells
최병태,김군도,최영현,Choi, Byung-Tae,Kim, Gun-Do,Choi, Yung-Hyun Korean Society of Life Science 2006 생명과학회지 Vol.16 No.4
The $Ca^{2+}-activated$ neutral protease calpain induced proteolysis has been suggested to play a role in certain cell growth regulatory proteins. Cyclin proteolysis is essential for cell cycle progression. D-type cyclins, which form an assembly with cyclin-dependent kinases (cdk4 and cdk6), are synthesized earlier in G1 of the cell cycle and seem to be induced in response to external signals that promote entry into the cell cycle. Here we show that cyclin D3 protein levels are regulated at the posttranscriptional level by calpain protease. Treatment of human breast carcinoma MDA-MB-231 cells with lovastatin and actinomycin D resulted in a loss of cyclin D3 protein that was completely reversible by the peptide aldehyde calpain inhibitor, LLnL. The specific inhibitor of the 26S proteasome, lactacystin, the lysosome inhibitors, ammonium chloride and chloroquine, and the serine protease inhibitor, phenylmethylsulfonylfluoride (PMSF), did not block the degradation of cyclin D3 by lovastatin and actinomycin D. Results of in vitro degradation of cyclin D3 by purified calpain showed that cyclin D3 protein is degraded in a $Ca^{2+}-dependent$ manner, and the half-life of cyclin D3 protein was dramatically increased in LLnL treated cells. These data suggested that cyclin D3 protein is regulated by the $Ca^{2+}-activated$ protease calpain. $Ca^{2+}$-농도 의존적으로 활성화되는 neutral protease calpain에 의한 단백질 분해는 세포의 성장을 조절하는데 중요한 단백질들의 역할에 매우 중요한 역할을 한다. Cyclin의 분해는 세포주기의 진행을 위한 필연적인 과정이다. D-type cyclins는 외부자극이나 신호에 의하여 세포주기의 G1 초기에 합성이 된 후 cyclin-dependent kinases (cdk4 및 cdk6)와의 결합하여 세포주기 S기 진입을 촉진하는 역할을 한다. 본 연구에서는 MDA-MB-231 인체 유방암세포에서 cyclin D3 단백질이 calpain protease에 의하여 전사 후 수준에서 조절 받고 있음을 제시하였다. 본 실험의 조건에서 lovastatin과 actinomycin D가 처리된 MDA-MB-231 세포에서 cyclin D3 단백질의 발현이 완전히 사라졌지만, calpain inhibitor인 LLnL의 처리에 의하여 정상 수준으로 회복되었음을 알 수 있었다. 그러나 26S proteasome의 선택적 억제제인 lactacystin, the lysosome 억제제인 ammonium chloride 및 chloroquine, serine protease 억제제인 PMSF는 동일 조건에서 lovastatin과 actinomycin D 처리에 의한 cyclin D3의 발현저하를 억제하지는 못하였다. In vitro 조건에서 순수 분리된 calpain은 cyclin D3 단백질을 $Ca^{2+}$ 농도 의존적으로 분해하였으며, cyclin D3 단백질의 half-life는 LLnL 처리에 의하여 매우 유의적으로 증가되었다. 이러한 결과는 cyclin D3 단백질이 $Ca^{2+}$에 의해 활성화 되는 protease calpain에 의해 조절됨을 보여준다.
Effects of Mycelial Extract of Phellinus linteus on Ethanol-Induced Liver Injury in Rats
최병태,최영현,길영기,Choi, Byung-Tae,Choi, Yung-Hyun,Gil, Young-Gi Korean Society of Life Science 2006 생명과학회지 Vol.16 No.6
상황버섯 배양균사체 추출물 (MCPL)이 알코올성 간 손상에 미치는 영향을 살펴보았다. Sprague-Dawley계 흰 쥐에 40% 알코올 3 ml을 MCPL (5 mg 및 15 mg/Kg)과 함께 1일 1회 10일간 투여하였다. 간 기능의 표지가 되는 혈청내 AST와 ALT값이 에탄올에 의해 현저히 증가하였으나 MCPL 투여에 의해 저하되며 특히 ALT 값이 유의성 있게 낮아졌다. 병리조직학적으로 살펴보면 알코올에 의해 염증세포의 침윤, 쿠퍼세포 반응 및 국소적 염증이 유발되나 MCPL투여에 의해 그 정도가 다소 완화되었다. 간소엽내 글리코겐 분포도 알코올에 의해 감소하나 MCPL투여에 의해 중심정맥주변 부위의 분포가 일부 회복되었다. 염증관련 단백질에 대한 Western blot 및 면역조직화학적 반응을 보면 에탄올 투여에 의해 COX-2, iNOS 및 $TNF-{\alpha}$ 면역반응이 증가하나 MCPL투여에 의해 발현의 감소를 볼 수 있었다. 이상의 결과로 보아 MCPL은 알코올에 의한 간 손상에 대해 보호 기능을 가짐을 알 수 있다. We investigated the anti-inflammatory effects of mycelial culture extract from Phellinus linteus (MCPL) for suppression in the process of ethanol-induced inflammation in rat liver. Levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly increased in the serum of ethanol-treated rats compared to normal. However, the level of ALT was arrested markedly in ethanol-treated rats with MCPL compared to ethanol alone treated control ones. Severe histopathological changes of liver such as cloudy swelling, inflammatory cells infiltration, Kupffer cell reaction and focal necrosis were demonstrated in the rats challenged with ethanol compared with normal. Fewer scores of these changes were observed in MCPL-treated rat with recovered glycogen in centrolobular region of hepatic lobule. The Western analysis showed that the expression of inflammatory proteins such as cyclooxygenase (COX)-1, COX-2, inducible nitric oxide synthase (iNOS), tumor necrosis factor $(TNF)-{\alpha}$ were increased in the ethanol-treated rat. But decline of COX-2 and iNOS expression were observed in MCPL-treated rat. Immunohistochemical analysis showed that the expression of COX-2 and $TNF-{\alpha}$ tended to increase in ethanol-treated rat, but decrease of these reactions were induced by MCPL treatment. These results suggest that MCPL may act as a protective agent for alcohol-induced liver injury through a regulating inflammation-related proteins.
상산의 $NF-{\kappa}B$ 활성억제작용과 $IKK{\gamma}$의 연관성 연구
최병태,이용태,황장선,문혜인,이경수,안원근,김동완,Choi, Byung-Tae,Lee, Yong-Tae,Hwang, Jang-Sun,Moon, Hae-In,Lee, Kyung-Soo,An, Won-Gun,Kim, Dong-Wan 대한동의생리학회 2006 동의생리병리학회지 Vol.20 No.6
Activation of $NF-{\kappa}B$ is known to be a trigger of various cellular disorders including inflammatory and autoimmune diseases such as rheumatoid arthritis. Numerous approaches are ongoing within laboratories to identify potential therapeutic agents which inhibit the $NF-{\kappa}B$ activation. In this study, we have tested the inhibitory effects of five traditional medicines on the activation of $NF-{\kappa}B$ by NIK. Among three medicines which exhibited inhibitory effect on the expression of $NF-{\kappa}B$ repoter plasmid, we investigated further the inhibitory mechanism of Dichroa febrifuga in connection with IKKY activity. Wild type $IKK{\gamma}$ inhibited the $NF-{\kappa}B$ activation by NIK but the C-terminal deletion mutant of IKKY did not show the inhibitory effect, indicating that the C-terminal leucine zipper domain of $NF-{\kappa}B$ is important for the inhibition of $NF-{\kappa}B$ activation. The water extract of Dichroa febrifuga(DFE) also strongly inhibited the $NF-{\kappa}B$ activation by NIK. The inhibitory activity of DFE appeared to be independent of the expression of $IKK{\gamma}$, suggesting that the pathways of inhibition by Dichroa febrifuga and $IKK{\gamma}$ are different. Our results suggest that Dichroa febrifuga can be used as a medicine for inhibition of the $NF-{\kappa}B$ activation in a wide range of cells without relation to the expression of $IKK{\gamma}$.
최병태(Byung Tae Choi),고우신(Woo Shin Ko),이용태(Yong Tae Lee),김경철(Gyeong Cheol Kim),이준혁(Jun Hyuk Lee),길영기(Young Gi Gil) 대한체질인류학회 1999 대한체질인류학회지 Vol.12 No.2
염증에서 iNOS 의 발현을 보기 위하여 흰쥐 정맥내 LPS 주사후 4시간,8 시간,12 시간에 뇌, 허파, 간, 심장을, 피부절제를 행한 후 5 일,10 일,15 일에 피부를 취하여 면역조직화학적으로 관찰하였다. LPS 주사군을 살펴보면 뇌에서 맥락엘기상피, 뇌실막세포에서 반응하며 일부 신경세포와 신경성유에서도 반응하는데 뇌들보와 시상하부에서 특히 높은 반응을 나타내었다. 허파에서는 허파파리큰포식세포, 허파꽈리세포, 민무늬근육세포 및 염증세포에서 반응이 나타났다. 간에서는 동굴모세혈관내 별큰포식세포와 더불어 염증세포에서 반응하며 일부 간세포와 쓸개관에서도 관찰되었다. 성장에서는 성장근육세포와 내피세포에서 관찰되었다. 이상의 반응은 LPS 투여후 8 시간에 높게 나타나며 뇌에서만 12 시 간에 다소 감소할뿐 다른 기관에서는 12 시간 까지 이러한 반응이 지속되었다. 피부에서는표피, 털뿌리의 상피뿌리집에서 반응을 나타내며 창상 치유 과정의 염증세포에서 강한 반응을 보이는데 특히 가피층아래 생괴사층에서 가장 강한 반응을 보였다. 반응정도는 창상치유 전과정에서 관찰되나 치유가 완료됨에 따라 줄어 들었다.