http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Saravanakumar, Kandasamy,Mandava, Suresh,Chellia, Ramachandran,Jeevithan, Elango,Babu Yelamanchi, Ravi Shankar,Mandava, Deepthi,Wen-Hui, Wu,Lee, Jongkook,Oh, Deog-Hwan,Kathiresan, Kandasamy,Wang, Myeo Elsevier 2019 Microbial pathogenesis Vol.126 No.-
<P><B>Abstract</B></P> <P>The present study aimed to purify and identify the metabolites from <I>T. atroviride</I> using high-performance liquid chromatography (HPLC) and <SUP>1</SUP>H and <SUP>13</SUP>C nuclear magnetic resonance spectrometer (NMR) followed by analyzing their toxicological, antibacterial and anticancer properties. This work identified two metabolites - TM1 and TM2. TM1 was in two forms: (i) 1, 3-dione-5, 5-dimethylcyclohexane; and, (ii) 2-enone-3hydroxy −5,5-dimethylcylohex, while TM2 was 4H-1,3-dioxin-4-one-2,3,6-trimethyl. These metabolites did not exhibit any irritant or allergic reaction as revealed by HET- CAM test. TM2 significantly inhibited the growth of <I>H. pylori</I> and Shigella toxin producing <I>Escherichia coli</I> (STEC) as evident by <I>in vitro</I> and microscopic observations of bacterial cell death. TM2 also induced the cell death and cytotoxicity, as revealed by cell viability test and western blot analysis. According to microscopic, flow cytometer and western blot analysis, TM2 treated cells displayed higher ROS, cell death, and apoptosis-related protein expression than TM1 and control. This study concluded that TM2 derived from <I>T. atroviride</I> was a potential therapeutic agent for anti-prostate cancer and antibiotic agent against MDR- <I>H. pylori</I> and STEC and it is also recommended to carry out further <I>in vivo</I> animal model experiments with improved stability of the metabolites for future pharmaceutical trails.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Fungal metabolites against <I>H. pylori</I> and Shigella toxin producing <I>Escherichia coli</I> (STEC). </LI> <LI> <I>Trichoderma</I> derived metabolites exhibited the antibacterial, and anticancer activity. </LI> <LI> TM2 reported as the potential therapeutic agent against - <I>H. pylori</I>, STEC, and anti-prostate cancer. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Potential Moracin M Prodrugs Strongly Attenuate Airway Inflammation In Vivo
( Jongkook Lee ),( Suresh Mandava ),( Sung-hoon Ahn ),( Myung-ae Bae ),( Kyung Soo So ),( Ki Sun Kwon ),( Hyun Pyo Kim ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.4
This study aims to develop new potential therapeutic moracin M prodrugs acting on lung inflammatory disorders. Potential moracin M prodrugs (KW01-KW07) were chemically synthesized to obtain potent orally active derivatives, and their pharmacological activities against lung inflammation were, for the first time, examined in vivo using lipopolysaccharide (LPS)-induced acute lung injury model. In addition, the metabolism of KW02 was also investigated using microsomal stability test and pharmacokinetic study in rats. When orally administered, some of these compounds (30 mg/kg) showed higher inhibitory action against LPSinduced lung inflammation in mice compared to moracin M. Of them, 2-(3,5-bis((dimethylcarbamoyl)oxy)phenyl)benzofuran-6-yl acetate (KW02) showed potent and dose-dependent inhibitory effect on the same animal model of lung inflammation at 1, 3, and 10 mg/kg. This compound at 10 mg/kg also significantly reduced IL-1β concentration in the bronchoalveolar lavage fluid of the inflamed-lungs. KW02 was rapidly metabolized to 5-(6-hydroxybenzofuran-2-yl)-1,3-phenylene bis(dimethylcarbamate) (KW06) and moracin M when it was incubated with rat serum and liver microsome as expected. When KW02 was administered to rats via intravenous or oral route, KW06 was detected in the serum as a metabolite. Thus, it is concluded that KW02 has potent inhibitory action against LPS-induced lung inflammation. It could behave as a potential prodrug of moracin M to effectively treat lung inflammatory disorders.
Samala, Mallesham,Lu, Thien Nhan,Mandava, Suresh,Hwang, Jungjoong,Bogonda, Ganganna,Kim, Donghoon,Park, Haeil,Kim, Deukjoon,Lee, Jongkook American Chemical Society 2018 ORGANIC LETTERS Vol.20 No.20
<P>A stereoselective protection-free asymmetric total synthesis of (+)-chamuvarinin (<B>1</B>), a potent anticancer and antitrypanosomal agent, has been accomplished. The adjacently linked [bis(tetrahydrofuran)]tetrahydropyran (THF-THF-THP) core of this natural product with seven stereogenic centers was constructed in a completely substrate-controlled fashion. The inter-ring stereochemistry (<I>threo,threo,threo</I>) of the oxatricyclic core was established in a stereoselective fashion by a chelation-controlled Keck allylation, whereas the intraring <I>cis</I> or <I>trans</I> relative stereochemistry was controlled by a stereoselective internal alkylation.</P> [FIG OMISSION]</BR>
Lee, Ji Hyun,Jung, Aeran,Park, Han Na,Lee, Changhee,Mandava, Suresh,Lim, Sung-jun,Lim, Byoung-bok,Park, Sung-Kwan,Lee, Jongkook,Kang, Hoil Elsevier 2018 Forensic Science International Vol.291 No.-
<P><B>Abstract</B></P> <P>Illicit psychoactive substances have threatened public health worldwide. An active metabolite of ADB-CHMINACA and MDMB-CHMINACA was identified for the first time in a powder-type product found in an airmail package. The structure of compound 1 was elucidated by a combination of gas chromatography-mass spectrometry (GC–MS), liquid chromatography-high resolution mass spectrometry (LC-HRMS), infrared (IR) spectroscopy, and nuclear magnetic resonance (NMR) spectroscopy. Compound 1 was proven to be an analogue of MDMB-CHMINACA, an indazole-based synthetic cannabinoid. The methyl ester group in MDMB-CHMINACA was replaced with a carboxylic acid group in compound 1. Compound 1 was determined as 2-[1-(cyclohexylmethyl)-1<I>H</I>-indazole-3-carboxamido]-3,3-dimethylbutanoic acid and named as DMBA-CHMINACA.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A new indazole-3-carboxamide class synthetic cannabinoid was identified. </LI> <LI> Compound 1 was named as DMBA-CHMINACA according to the EMCDDA guideline. </LI> <LI> DMBA-CHMINACA is a hydrolysed form of MDMB-CHMINACA. </LI> <LI> DMBA-CHMINACA is a potential CB1 and CB2 agonist. </LI> <LI> DMBA-CHMINACA can work as a synthetic precursor of several synthetic cannabinoids. </LI> </UL> </P>