• Natural Product Sciences
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• 제10권3호
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• pp.129-133
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• 2004

Quercetin is a dietary anticancer chemical that is capable of inducing apoptosis in tumor cells. However, little is known about its biological effect in nonmalignant hepatic cells. Using embryonic normal hepatic cell line (BNL CL.2) and its SV40-transformed tumorigenic cell line (BNL SV A.8), we evaluated the effects of quercetin on cell proliferation and apoptosis. As the results, our present study demonstrated that quercetin had a selective growth inhibition in normal versus tumorigenic hepatic cells such that BNL SV A.8 cells were very sensitive to the quercetin-mediated cytotoxicity. In particular, as evidenced by the increased number of positively stained cells in the TUNEL assay, the induction of characteristic nuclear DNA ladders, and the migration of many cells to sub-G1 phase in the BNL SV A.8 cells, quercetin treatment more sensitively induced apoptosis in BNL SV A8 cells than in BNL CL.2 cells. Collectively, our findings suggest that quercetin can be approached as a potential agent that is capable of inducing selective growth inhibition and apoptosis of hepatic cancer cells.

• Journal of Microbiology and Biotechnology
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• 제29권1호
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• pp.59-65
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• 2019

Fusaricidin analogs, produced by Paenibacillus polymyxa, were tested for selective control of a major bloom-forming cyanobacterium, Microcystis sp. Fusaricidin (A and B mixtures) and four analogs were isolated from P. polymyxa E681 and investigated for their inhibition of cyanobacterial cell growth. Among the four fusaricidin analogs, fraction 915 Da (designated as Fus901) showed growth inhibition activity for Microcystis aeruginosa but not for Anabaena variabilis and Scenedesmus acutus. Microcystin concentration decreased up to 70% and its content per cell also decreased over 50% after 3 days. Fusaricidin exhibited growth inhibition against Gram-positive bacteria but Fus901 did not. Molecular weights of fusaricidin A and B were 883 Da and 897 Da, whereas that of Fus901 was 915 Da. Structure analysis by a ring-opening method revealed a linear form for Fus901. Expression of the pod gene related to oxidative stress was increased 2.1-fold by Fus901 and that of mcyD decreased up to 40%. These results indicate that Fus901 exerts oxidative stress against M. aeruginosa. Thus, Fus901 can be used as a selective cyanobactericide without disturbing the ecological system and could help in decreasing the microcystin concentration.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.244.1-244.1
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• 2002

Cyclooxygenase-2 ( COX-2 ) is an inducible enzyme which produces prostanoids by various stimuli. Overexpression of COX-2 in many tumor types indicates its association with tumor progression, which has been a promising target for chemoprevention and chemomodulation. We studied conc- and time-dependency of COX-2 inhibition, growth inhibition, and cell cycle arrest induced by celecoxib, a selective COX-2 inhibitor, in human non-small cell lung cancer (NSCLC) A549 cells. (omitted)

• Maxillofacial Plastic and Reconstructive Surgery
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• 제30권4호
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• pp.333-344
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• 2008

The objectives of this study was to explore the growth pattern of the oral squamous cell carcinoma when overexpressed COX was inhibited, explore the pathway that COX inhibitors suppressed the proliferation of cancer cells, and then hereafter investigate the potential of COX as chemopreventive target for oral squamous cell carcinoma. For confirming the COX-dependent effect and mechanisms on growth of the oral cancer cells, we treated the nonselective NSAID, Mefenamic acid and COX-2 selective inhibitor, Celecoxib in HN4 cell line. And then the cell line was evaluated with MTT assay and growth curve, the production of PGE2, total RNA extraction and RT-PCR analysis, and TEM The results were obtained as follows: 1. After administration of medication, in the result of MTT assay, Celecoxib inoculated group inhibit the cell growth rather than Mefenamic acid inoculated group. 2. The growth curve of cell line showed as time passes by there was a dramatic cell growth in the control group, and gradual growth inhibition was found in medication inoculated group and, in Celecoxib inoculated group there was more inhibition of cell growth. 3. After the administration of medication, Celecoxib tend to inhibit the synthesis of PGE2 more than Mefenamic acid. Mefenamic acid inhibit the synthesis of PGE2 more as the concentration gets high, but Celecoxib inhibited the synthesis of PGE2 even in low concentration. 4. After the administration of medication, the revelation of COX mRNA in cell line, there was a 50% decrease in COX-1, 60% decrease in COX-2 as in $50{\mu}M$ Mefenamic acid, and in Celecoxib $50{\mu}M$ there was not much difference in COX-1 and 90% decrease in COX-2 was found. 5. HN4 cell line showed broken nucleus and tangled cytoskeleton bundles in cytoplasm which meant apoptotic features after the treatment of Celecoxib in TEM view. Depending on the above results, we estimate that the inhibition of the expression of COX-2 cause the growth suppression of the oral squamous cell carcinoma, and it get achieved through pathway of reduced PGE2 production and increased apoptosis. In addition to, because COX-2 selective inhibitor specifically act to COX-2, it is considered that COX-2 selective inhibitor has the adequate potential as chemopreventive agent for oral squamous cell carcinoma.

• 한국미생물·생명공학회지
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• 제23권2호
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• pp.214-219
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• 1995

In fermentation of dairy products, bifidobacteria is used in conjunction with other lactic acid bacteria, such as L. acidophilus, L. bulgaricus and S. thermophilus, rendering the enumeration of bifidobacteria difficult. In order to develop optimum conditions for selective enumeration of bifidobacteria, we examined MIC of several antibiotics against various bifidobacteria and other lactic acid bacteria. The growth of L. acidophilus, L. bulgaricus and S. thermophilus were inhibited by lithium chloride at the concentration of less than 4 mg/ml, whereas growth inhibition of bifidobacteria occurred at concentrations over 6-10 mg/ml. Tetracycline and chloramphenicol were also found to selectively inhibit growth of other lactic acid bacteria at the concentration of 1-3 $\mu$g/ml. Addition of 6 mg/ml lithium chloride, 1 $\mu$g/ml, tetracycline or 3 $\mu$g/ml chloramphenicol to medium was found to be optimal for selective enumeration of bifidobacteria. By using these three inhibitory chemicals in the TPY medium, higher number of bifidobacteria were selectively isolated than with NPNL agar and LP agar.

• 대한약침학회지
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• 제20권3호
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• pp.207-212
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• 2017

Objectives: Study of the mechanisms involved in cancer progression suggests that cyclooxygenase enzymes play an important role in the induction of inflammation, tumor formation, and metastasis of cancer cells. Thus, cyclooxygenase enzymes could be considered for cancer chemotherapy. Among these enzymes, cyclooxygenase 2 (COX-2) is associated with liver carcinogenesis. Various COX-2 inhibitors cause growth inhibition of human hepatocellular carcinoma cells, but many of them act in the COX-2 independent mechanism. Thus, the introduction of selective COX-2 inhibitors is necessary to achieve a clear result. The present study was aimed to determine the growth-inhibitory effects of new analogues of chalcone epoxide as selective COX-2 inhibitors on the human hepatocellular carcinoma (HepG2) cell line. Methods: Estimation of both cell growth and the amount of prostaglandin E2 (PGE2) production were used to study the effect of selective COX-2 inhibitors on the hepatocellular carcinoma cell. Cell growth determination has done by MTT assay in 24 h, 48 h and 72 h, and PGE2 production has estimated by using ELYSA kit in 48 h and 72 h. Results: The results showed growth inhibition of the HepG2 cell line in a concentration and time-dependent manner, as well as a reduction in the formation of PGE2 as a product of COX-2 activity. Among the compounds those analogues with methoxy and hydrogen group showed more inhibitory effect than others. Conclusion: The current in-vitro study indicates that the observed significant growth-inhibitory effect of chalcone-epoxide analogues on the HepG2 cell line may involve COX-dependent mechanisms and the PGE2 pathway parallel to the effect of celecoxib. It can be said that these analogues might be efficient compounds in chemotherapy of COX-2 dependent carcinoma specially preventing and treatment of hepatocellular carcinomas.

• Journal of Microbiology and Biotechnology
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• 제20권8호
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• pp.1240-1242
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• 2010

We attempted to identify the compound responsible for the growth inhibition of Microcystis aeruginosa occurring when a culture broth of Bacillus subtilis C1 was added to the medium. The active compound was purified from B. subtilis C1 culture broth by adsorption chromatography and HPLC, and was identified as a type of glycolipid based on $^1H$ NMR and MS analyses. The purified active compound completely inhibited the growth of M. aeruginosa at a concentration of 10 ${\mu}g/ml$. This is the first report of a glycolipid produced by a Bacillus strain that has potential as an agent for the selective control of bloom-forming M. aeruginosa.

• 한국잡초학회지
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• 제7권2호
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• pp.220-235
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• 1987

본연구(本硏究)는 벼품종(品種) 및 주요(主要) 논 잡초종(雜草種)에 대(對)한 Oxyfluorfen의 선택활성차이(選擇活性差異)를 구명(究明)하여 수도(水稻) 포장(圃場)에서의 이용가능성(利用可能性)을 살펴 보고자 수행(遂行)되었으며 결과(結果)를 요약(要約)하연 다음과 같다. 1. Oxyf1uorfen의 발생전처리(發生前處理)에서 너도방동사니를 포함(包含)한 공시잡초종(供試雜草種)과 벼와의 선택활성차이(選擇活性差異)는 $ED_{50}$으로 보아 0.1~0.4 kg a. i./ha 수준(水準)에서 성립(成立)되었다. 2. $10^{-5}$ M Oxyfluorfen의 발생후처리(發生後處理)에서 생육(生育)의 억제(抑制)는 전체처리(全體處理)>뿌리처리(處理)>경부대상처리(莖部帶狀處理) 순(順)으로 심(甚)하였으며, 특(特)히 너도방동사니와 벼에서는 생육억제(生育抑制)가 경미(輕微)하였다. 3. 광합성(光合成)의 저해(沮害)는 공시초종(供試草種) 모두, $10^{-4}$ M Oxyfluorfen 농도(濃度)에 서부터 심(甚)하게 나타났으며 호흡저해(呼吸沮害)의 차이(差異)는 인정(認定)되지 않았다. 4. 유리단세포(遊離單細胞)에서 Oxyfluorfen 처리시(處理時) 벼 2 품종(品種)과 너도방동사니가 $10^{-5}$ M 농도수준(濃度水準)에서 내성(耐性)을 보인 반면 피와 올미는 상대적(相對的)으로 감수성(感受性)을 보였다. 5. 벼의 현탁배양(懸濁培養)에서 세포(細胞)의 생장(生長)은 Oxyfluorfen의 농도증가(濃度增加)에 따라 억제(抑制)되었으며 Aichiasahi 보다 Mushakdanti 에서 크게 억ㅈ(抑制)되었다.

• 대한한방종양학회지
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• 제5권1호
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• pp.137-150
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• 1999

Macrophage play a major role in host defence against infection and tumor development and this activity is regulated through the production of several mediators. In particular, the production of NO by macrophages mediates killing or growth inhibition of tumor cells, bacteria, fungi and parasites. However, over-expression of iNOS by various stimuli, resulting in over-production of NO, contributes to the pathogenesis of septic shock and some inflammator and auto-immune disease. Therefore, it would be valuable to develop potent and selective inhibitors of for potential therapeutic use. Thus the agent that supprees the expression of iNOS mRNA or enzyme protein will be usefull for the prevention of various diseases. We are intersted in identifying selective inhibitiors of iNOS which might be useful intreating inflammatory human diseases. In summary, we have demenstrated that scopoletin, isolated from Seman Armenicae and Radix Trichosanthis the production of NO induced by $IFN-\gammer$ plus LPS in RAW 264.7 macrophages, The mechanism for the inhibition of NO production was due to suppression of the expression of iNOS mRNA or enzyme protein.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.599-607
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• 2017

Most normal cells express L-type amino acid transporter 2 (LAT2). However, L-type amino acid transporter 1 (LAT1) is highly expressed in many tumor cells and presumed to support their increased growth and proliferation. This study examined the effects of JPH203, a selective LAT1 inhibitor, on cell growth and its mechanism for cell death in Saos2 human osteosarcoma cells. FOB human osteoblastic cells and Saos2 cells expressed LAT1 and LAT2 together with their associating protein 4F2 heavy chain, but the expression of LAT2 in the Saos2 cells was especially weak. JPH203 and BCH, a non-selective L-type amino acid transporter inhibitor, potently inhibited L-leucine uptake in Saos2 cells. As expected, the intrinsic ability of JPH203 to inhibit L-leucine uptake was far more efficient than that of BCH in Saos2 cells. Likewise, JPH203 and BCH inhibited Saos2 cell growth with JPH203 being superior to BCH in this regard. Furthermore, JPH203 increased apoptosis rates and formed DNA ladder in Saos2 cells. Moreover, JPH203 activated the mitochondria-dependent apoptotic signaling pathway by upregulating pro-apoptotic factors, such as Bad, Bax, and Bak, and the active form of caspase-9, and downregulating anti-apoptotic factors, such as Bcl-2 and Bcl-xL. These results suggest that the inhibition of LAT1 activity via JPH203, which may act as a potential novel anti-cancer agent, leads to apoptosis mediated by the mitochondria-dependent intrinsic apoptotic signaling pathway by inducing the intracellular depletion of neutral amino acids essential for cell growth in Saos2 human osteosarcoma cells.