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( Sabina Shrestha ),( Ji Hae Park ),( Dae Young Lee ),( Jin Gyeong Cho ),( Do Gyeong Lee ),( Moon Hee Cho ),( Tae Sook Jeong ),( Hee Cheol Kang ),( Nam In Baek ) 한국응용생명화학회 2011 Journal of Applied Biological Chemistry (J. Appl. Vol.54 No.1
The bark of Machilus thunbergii was extracted with 80% aqueous methanol (MeOH), and the concentrated extract was partitioned using ethyl acetate (EtOAc), butanol (n-BuOH), and H2O, successively. From the EtOAc fraction, five lignans were isolated through the repeated silica gel, octadecyl silica gel (ODS) and, Sephadex LH-20 column chromatography. Based on nuclear magnetic resonance (NMR), mass spectroscopy (MS), and infrared spectroscopy (IR) spectroscopic data, the chemical structures of the compounds were determined to be machilin A (1), machilin F (2), licarin A (3), nectandrin A (4), and nectandrin B, (5). This study presents comparative account of five lignans from M. thunbergii bark contributing inhibition of low density lipoprotein (LDL), ACAT-1, and ACAT-2. Compounds 2-5 showed varied degree of antioxidant activity on LDL with IC50 values of 2.1, 11.8, 15.3, and 4.1 μM. Compounds 1, 2, and 3 showed inhibition activity on ACAT-1 with values 63.4±6.9% (IC50=66.8 μM), 53.7±0.9% (IC50=109.2 μM), and 78.7±0.2% (IC50= 40.6 μM), respectively, at a concentration of 50 mg/mL, and on ACAT-2 with values 47.3±1.5% (IC50=149.7 μM), 39.2±0.2% (IC50=165.2 μM), and 52.1±1.0% (IC50=131.0 μM), respectively, at a concentration of 50 mg/mL.
( Mi Young Baek ),( Jin Gyeong Cho ),( Dae Young Lee ),( Eun Mi Ahn ),( Tae Sook Jeong ),( Nam In Baek ) 한국응용생명화학회 2010 Applied Biological Chemistry (Appl Biol Chem) Vol.53 No.3
The dried stem bark of Albizia julibrissin was extracted in 70% aqueous EtOH, and concentrated extracts were partitioned with EtOAc, n-BuOH, and H2O, successively. From the EtOAc fraction, three triterpenoids were isolated through repeated silica gel and octadecyl silica gel column chromatography. Based on nuclear magnetic resonance spectrometry (NMR), mass spectrometry, and infrared spectroscopy spectroscopic data, the chemical structures of the compounds were determined to be lupeol (1), betulinic acid (2), and oleanolic acid (3). This was the first report in which compounds 1, 2, and 3 were isolated from the stem bark of A. julibrissin. Since the NMR data for some compounds have been incorrectly or incompletely identified in previous literature, the NMR were revised on the basis of 2-D NMR experiments. Compounds 1, 2, and 3 showed inhibition activity on ACAT-1 with values of 89.3±3.7%, 61.2±3.4%, and 52.5±0.7%, respectively, at a concentration of 50 μg/mL and on ACAT-2 with values of 44.3±2.1%, 55.5±0.3%, and 22.0±2.6%, respectively, at a concentration 50 μg/mL.
Baek, Mi-Young,Cho, Jin-Gyeong,Lee, Dae-Young,Ahn, Eun-Mi,Jeong, Tae-Sook,Baek, Nam-In The Korean Society for Applied Biological Chemistr 2010 Applied Biological Chemistry (Appl Biol Chem) Vol.53 No.3
The dried stem bark of Albizia julibrissin was extracted in 70% aqueous EtOH, and concentrated extracts were partitioned with EtOAc, n-BuOH, and $H_2O$, successively. From the EtOAc fraction, three triterpenoids were isolated through repeated silica gel and octadecyl silica gel column chromatography. Based on nuclear magnetic resonance spectrometry (NMR), mass spectrometry, and infrared spectroscopy spectroscopic data, the chemical structures of the compounds were determined to be lupeol (1), betulinic acid (2), and oleanolic acid (3). This was the first report in which compounds 1, 2, and 3 were isolated from the stem bark of A. julibrissin. Since the NMR data for some compounds have been incorrectly or incompletely identified in previous literature, the NMR were revised on the basis of 2-D NMR experiments. Compounds 1, 2, and 3 showed inhibition activity on ACAT-1 with values of $89.3{\pm}3.7%$, $61.2{\pm}3.4%$, and $52.5{\pm}0.7%$, respectively, at a concentration of $50\;{\mu}g/mL$ and on ACAT-2 with values of $44.3{\pm}2.1%$, $55.5{\pm}0.3%$, and $22.0{\pm}2.6%$, respectively, at a concentration $50\;{\mu}g/mL$.
Mi Young Baek,Jin Gyeong Cho,Dae Young Lee,Eun Mi Ahn,Tae Sook Jeong,Nam In Baek 한국응용생명화학회 2010 Journal of Applied Biological Chemistry (J. Appl. Vol.53 No.3
The dried stem bark of Albizia julibrissin was extracted in 70% aqueous EtOH, and concentrated extracts were partitioned with EtOAc, n-BuOH, and H2O, successively. From the EtOAc fraction, three triterpenoids were isolated through repeated silica gel and o
신생아 스크리닝으로 진단된 Alpha-methylacetoacetic Aciduria 증례
이범희,김유미,김재민,김구환,유한욱,Lee, Beom Hee,Kim, Yoo-Mi,Kim, Jae-Min,Kim, Gu-Hwan,Yoo, Han-Wook 대한유전성대사질환학회 2012 대한유전성대사질환학회지 Vol.12 No.2
본 연구는 신생아 대사 이상 질환에 대한 광범위 스크리닝으로 매우 희귀한 아미노산 대사 이상 질환 중 하나인 Alpha-methylacetoacetic aciduria의 국내 첫 증례를 경험했기에 이를 보고하는 바이다. 신생아 스크리닝의 광범위한 시행으로 인해 향후 우리나라에도 알려지지 않은 희귀 유전성 대사 질환의 보고가 증가할 것으로 예측된다. 이 환자들에 대한 적절한 관리를 통해 질환의 자연경과와 장기적 예후에 대한 관찰이 필요하다. Alpha-methylacetoacetic aciduria is a rare inborn metabolic disorder, caused by acetyl-CoA acetyltransferase-1 deficiency. This enzyme acts on the last step of isoleucine metabolism. It dissociates 2-Methyl-3-Hydroxybutyryl-CoA into propionyl-CoA and acetyl-CoA. ACAT1 is the causative gene. Most patients manifest recurrent ketotic metabolic acidosis, but some patients can be identified in their presymptomatic period by newborn screening. Urinary organic acid profile is characterized by increased amounts of 2-Methyl-3-Hydroxybutyric acid, tiglylglycine, and 2-methyl acetoacetic acid. In this report, a Korean patient with alpha-methylacetoacetic aciduria is described. This is the first Korean case report confirmed by genetic testing.
Jin, Ying-Lan,Rho, Mun-Chual,Gajulapati, Kondaji,Jung, Hwa-Young,Boovanahalli, Shanthaveerappa K.,Lee, Jee-Hyun,Song, Gyu-Yong,Choi, Jung-Ho,Kim, Young-Kook,Lee, Kyeong,Choi, Yong-Seok Korean Chemical Society 2009 Bulletin of the Korean Chemical Society Vol.30 No.6
A novel series of imidazo[1,2-$\alpha$]pyridines was designed, synthesized, and tested for their ability to inhibit acyl- CoA:cholesterol acyltransferase. Preliminary lead optimization efforts resulted in the identification of ACAT inhibitors represented by analogues 5b, 5c, 6a, 6c, 7b, and 7c. The ACAT inhibitory activity of these compounds was further established by potent inhibition of cholesteryl ester formation in HepG2 cells by a representative analogue 7b.
Yinglan Jin,노문철,Kondaji Gajulapati,Hwa Young Jung,Shanthaveerappa K. Boovanahalli,이지현,Jung Ho Choi,김영국,Kyeong Lee,Yongseok Choi 대한화학회 2009 Bulletin of the Korean Chemical Society Vol.30 No.6
A novel series of imidazo[1,2-α]pyridines was designed, synthesized, and tested for their ability to inhibit acyl- CoA:cholesterol acyltransferase. Preliminary lead optimization efforts resulted in the identification of ACAT inhibitors represented by analogues 5b, 5c, 6a, 6c, 7b, and 7c. The ACAT inhibitory activity of these compounds was further established by potent inhibition of cholesteryl ester formation in HepG2 cells by a representative analogue 7b.