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Li, Hong-Mei,Jang, Ji Hye,Jung, Jun-Sub,Shin, Jiseon,Park, Chul O.,Kim, Yeon-Ja,Ahn, Won-Gyun,Nam, Ju-Suk,Hong, Chang-Won,Lee, Jongho,Jung, Yu-Jin,Chen, Jiang-Fan,Ravid, Katya,Lee, H. Thomas,Huh, Won- American Association of Immunologists 2019 Journal of Immunology Vol. No.
<P>G2A is a GPCR abundantly expressed in immune cells. G2A<SUP>−/−</SUP> mice showed higher lethality, higher plasma cytokines, and an impaired bacterial clearance in response to a murine model of sepsis (cecal ligation and puncture), which were blocked by GdCl<SUB>3</SUB>, an inhibitor of Kupffer cells. Anti–IL-10 Ab reversed the impaired bacterial clearance in G2A<SUP>−/−</SUP> mice. Indomethacin effectively blocked both the increased i.p. IL-10 levels and the impaired bacterial clearance, indicating that disturbed PG system is the proximal cause of these phenomena. Stimulation with LPS/C5a induced an increase in <I>Escherichia coli</I> phagocytosis and intracellular cAMP levels in G2A<SUP>+/+</SUP> peritoneal macrophages but not G2A<SUP>−/−</SUP> cells, which showed more PGE<SUB>2</SUB>/nitrite release and intracellular reactive oxygen species levels. Heterologous coexpression of G2A and adenosine receptor type 2b (A2bAR) induced a synergistic increase in cAMP signaling in a ligand-independent manner, with the evidence of physical interaction of G2A with A2bAR. BAY 60-6583, a specific agonist for A2bAR, increased intracellular cAMP levels in Kupffer cells from G2A<SUP>+/+</SUP> but not from G2A<SUP>−/−</SUP> mice. Both G2A and A2bAR were required for antiseptic action of lysophosphatidylcholine. These results show inappropriate activation of G2A<SUP>−/−</SUP> Kupffer cells to septic insults due to an impaired cAMP signaling possibly by lack of interaction with A2bAR.</P>
Enzymatic synthesis of novel isobavachalcone glucosides via a UDP-glycosyltransferase
Hong-Mei Li,이재경,Li-Juan Nie,Qiang Huo,Tao Ma,송재경,홍영수,Cheng-Zhu Wu 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.12
Glycosylation is often used to improve a natural product’s properties such as water solubility, chemical stability, pharmacological potency, and structure diversification. In this study, we studied the enzymatic synthesis of novel isobavachalcone glucosides using a UDP-glycosyltransferase (YjiC) from Bacillus licheniformis DSM-13. The chemical structures of compounds 1 and 2 were elucidated by spectroscopic techniques, including LC–MS, MS, and NMR. Meanwhile, the parameters of glycosylation reaction such as incubation time, UDP-glucose concentration, and pH of buffer were also optimized during this study. Furthermore, the compounds 1 and 2 exhibited weak anti-proliferative activities against five human cancer cell lines, with IC50 values ranging from 58.6 to 86.6 lM.
Magnolol Inhibits iNOS, p38 Kinase, and NF-κB/Rel in Murine Macrophages
Li Mei Hong,Chang In-Youp,Youn Ho-Jin,Jang Dae-Sik,Kim Jin-Sook,Jeon Young-Jin Korean Society of ToxicologyKorea Environmental Mu 2006 Toxicological Research Vol.22 No.3
We demonstrate that magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells(murine macrophage cell line). Treatment of RAW 264.7 cells with magnolol inhibited LPS-stimulated nitric oxide production in a dose-related manner. RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression. Western immunoblot analysis of phosphorylate p38 kinase showed magnolol significantly inhibited the phosphorylation of p38 kinase which is important in the regulation of iNOS gene expression. The specific p38 inhibiter SB203580 abrogated the LPS-induced NO generation and iNOS expression, whereas the selective MEK-1 inhibitor PD98059 did not affect the NO induction. Immunostaining of p65 and reporter gene assay showed that magnolol inhibited NF-${\kappa}/Rel$ nuclear translocation and transcriptional activation, respectively. Collectively, this series of experiments indicates that magnolol inhibits iNOS gene expression by blocking NF-k/Rel and p38 kinase signaling. Due to the critical role that NO release plays in mediating inflammatory responses, the inhibitory effects of magnolol or iNOS suggest that magnolol may represent a useful anti-inflammatory agent.
Pretreatment of Macrophages with Paclitaxel Inhibits iNOS Expression
Li Mei-Hong,Kang Jong-Soon,Kim Hwan-Mook,Jeon Young-Jin Korean Society of ToxicologyKorea Environmental Mu 2006 Toxicological Research Vol.22 No.2
We demonstrate that paclitaxel, an antitumor agent derived from yew tree, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Previously, paclitaxel has been known to induce iNOS gene expression in macrophages. However, in this report we described that the pre-treatment of macrophages with paclitaxel ($0.1{\mu}M$) for 8 h inhibited LPS-induced iNOS gene expression. Pretreatment of RAW 264.7 cells with paclitaxel significantly inhibited LPS-stimulated nitric oxide (NO) production. Western immunoblot of iNOS and RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunocytochemical staining of iNOS further confirmed that pretreatment of macrophages with paclitaxel inhibited macrophage activation. Electrophoretic mobility shift assay showed that paclitaxel inhibited $NF-_{\kappa}/Rel$ DNA binding. Collectively, these series of experiments indicate that paclitaxel inhibits iNOS gene expression by blocking $NF-_{\kappa}B/Rel$ activation.
HONG, SANG-WON,JUNG, KYUNG HEE,CHOI, MYUNG-JOO,KIM, DA YOUNG,LEE, HEE-SEUNG,ZHENG, HONG-MEI,LI, GUANG YONG,EL-DEEB, IBRAHIM M.,PARK, BYUNG SUN,LEE, SO HA,HONG, SOON-SUN Spandidos Publications 2012 International journal of oncology Vol.41 No.5
<P>The anticancer effect of a new pyrazole derivative, KI-10F (2-(4-(2-(4-(dimethylamino) phenyl)pyridin-4-yl)-5-(3-methoxy-5-methylphenyl)-1H-pyrazol?1-yl) acetonitrile)?3.5HCl) was evaluated in human colon cancer cells. KI-10F strongly suppressed the growth of human colon cancer cells and induced apoptosis by increasing the proportion of sub-G1 presenting apoptotic cells as well as causing cell cycle arrest at the G2/M phase. Apoptosis by KI-10F was confirmed by observation of an increase in the expression of cleaved caspase-3, caspase-8, caspase-9 and Bax, and the decrease of Bcl-2. Decreased expression of HIF-1α and VEGF, and the inhibition of HUVEC tube formation and migration showed that KI-10F effectively inhibited the angiogenesis process. Furthermore, in?vivo study in a mouse xenograft model showed that KI-10F produced a stronger antitumor activity than 5-FU, a conventional anticancer drug prescribed for the treatment of colon cancer. The effects of KI-10F on tumor proliferation (PCNA), angiogenesis (CD34) and apoptosis (cleaved caspase-3) were evaluated by immunohistochemistry using isolated tumor tissue samples. Taken together, our results demonstrated that KI-10F induces apoptosis and inhibits cell growth and angiogenesis both in?vitro and in?vivo. We suggest that KI-10F is an effective chemotherapeutic candidate for use against colon cancer.</P>
Li, Hong-Yuan,Li, Shan-Shan,Liu, Dian-Li,Dong, Yan-Mei,Tian, Wen-Jing Kyung Hee Oriental Medicine Research Center 2003 Oriental pharmacy and experimental medicine Vol.3 No.2
Respiratory syncytial virus (RSV) has long been considered an important cause of severe lower respiratory tract infection in infants and young children throughout the world. Unfortunately, no effective treatment of RSV exists. Therefore, New agents are needed to reduce the impact of RSV. We have studied the anti-viral effect of traditional Chinese midicinal herbs for over ten years and find Herba Patrinea (a Chinese medicinal herb) has the anti-RSV effect in vitro. In this study, the Herba Patrinea was extracted with hot water, condensed and sterilized. The cytotoxicity of the aqueous extract was tested by adding the diluted extract directly to HeLa cells and its effect on anti-RSV was estimated by the CPEI assay. As a result, the median cytotoxic concentration $(CC_{50})$ of Herba Patrinea was 32 mg/ ml by morphological observation, the median effective concentration (50% effective concentration, $EC_{50}$) of the Herba Patrinea against replication of the Long strain of RSV in HeLa cells were 1.25 mg/ml. The selectivity index $(SI=CC_{50}/EC{50})$ is 25.6. Moreover, Herba Patrinea gave a dose-dependent response in inhibiting RSV. In time of addition experiment, Herba Patrinea inhibited replication of RSV in HeLa cells when it was added at 0h, 2h, and 4h after virus infection. In summary, the results of this study suggest Herba Patrinea may be a novel anti-RSV drug and it is worthy of further studying.
Pretreatment of Macrophages with Paclitaxel Inhibits iNOS Expression
Mei Hong Li,Jong Soon Kang,Hwanmook Kim,Young Jin Jeon 한국독성학회 2006 Toxicological Research Vol.22 No.2
We demonstrate that paclitaxel, an antitumor agent derived from yew tree, inhibits LPS-induced expression of iNOS gene in RAW 264.7 cells. Previously, paclitaxel has been known to induce iNOS gene expression in macrophages. However, in this report we described that the pretreatment of macrophages with paclitaxel (0.1 μM) for 8 h inhibited LPS-induced iNOS gene expression. Pretreatment of RAW 264.7 cells with paclitaxel significantly inhibited LPS-stimulated nitric oxide (NO) production. Western immunoblot of iNOS and RT-PCR analysis showed that the decrease of NO was due to the inhibition of iNOS gene expression in RAW 264.7 cells. Immunocytochemical staining of iNOS further confirmed that pretreatment of macrophages with paclitaxel inhibited macrophage activation. Electrophoretic mobility shift assay showed that paclitaxel inhibited NF-κ/Rel DNA binding. Collectively, these series of experiments indicate that paclitaxel inhibits iNOS gene expression by blocking NF-κB/Rel activation.
Hong Mei Li,김진규,Jai Man Jang,Cheng-Bi Cui,임순성 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.9
We isolated five phenolic glycosides (acteoside,eutigoside B, isoacteoside, rutin and cornoside) fromAbeliophyllum distichum leaves by high-speed countercurrent chromatography (HSCCC) using a solvent systemof ethyl acetate:n-butanol:water (8:0.7:5). We determinedthe purity of the 5 compounds by high-performance liquidchromatography, and confirmed their chemical structuresby using nuclear magnetic resonance data. We examinedthe inhibitory effect of these compounds on rat lens aldosereductase. Among these compounds, acteoside (1) showedthe most potent inhibitory effect, with an IC50 value of1.39 lM. The inhibitory effect of 1 was 5.0 times greaterthan that of quercetin (7.05 lM), which was used as apositive control. These results suggest that acteoside maybe a promising agent for the prevention or treatment ofdiabetic complications. Moreover, HSCCC is a promisingmethod for the isolation and purification of biologicallyactive compounds from natural products.