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Abekura, Fukushi,Park, Junyoung,Kwak, Choong-Hwan,Ha, Sun-Hyung,Cho, Seung-Hak,Chang, Young-Chae,Ha, Ki-Tae,Chang, Hyeun-Wook,Lee, Young-Choon,Chung, Tae-Wook,Kim, Cheorl-Ho Elsevier 2019 INTERNATIONAL IMMUNOPHARMACOLOGY Vol.68 No.-
<P><B>Abstract</B></P> <P>Natural compound esculentoside B (EsB), (2S,4aR,6aR,6aS,6bR,8aR,9R,10R,11S,12aR,14bS)-11-hydroxy-9-(hydroxymethyl)-2 methoxycarbonyl-2,6a,6b,9,12a-pentamethyl-10-[(2<I>S</I>,3<I>R</I>,4<I>S</I>,5<I>R</I>)-3,4,5-trihydroxyoxan-2-yl]oxy-1,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid with molecular weight of 664.833, isolated from roots of <I>Phytolacca acinosa</I> Roxb has been widely used as a constituent of traditional Chinese medicine (TCM). However, the anti-inflammatory capacity of EsB has not been reported yet. Therefore, the objective of this study was to investigate anti-inflammatory activities of EsB in LPS-treated macrophage RAW 264.7 cells. EsB could inhibit nitric oxide (NO) production. EsB also suppressed gene and protein expression levels of inducible isoform of NO synthase (NOS) and cyclooxygenase-2 in a dose-dependent manner. In addition, EsB decreased gene expression and protein secretion levels of pro-inflammatory cytokines such as IL-1β, TNF-α, and IL-6. EsB remarkably suppressed nuclear translocation of nuclear factor kappa-B (NF-κB) from cytosolic space. Phosphorylation of IκB was also inhibited by EsB. Moreover, EsB specifically down-regulated phospho-c-Jun N-terminal kinase (p-JNK), but not p-p38 or phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2). Taken together, these results suggest that EsB has inhibitory effect on inflammatory response by inactivating NF-κB and p-JNK. It could be used as a new modulatory drug for effective treatment of inflammation-related diseases.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Natural compound esculentoside B (EsB) is isolated from roots of <I>Phytolacca acinosa</I> Roxb. </LI> <LI> EsB has inhibitory effect on inflammatory response by inactivating NF-κB and p-JNK. </LI> <LI> EsB is potentially effective as an anti-inflammatory agent to prevent and treat inflammatory responses. </LI> </UL> </P>
Lee, Miri,Kim, Kyoung-Sook,Fukushi, Abekura,Kim, Dong-Hyun,Kim, Cheorl-Ho,Lee, Young-Choon MDPI 2018 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.19 No.7
<P>Curcumin, a natural polyphenolic compound isolated from the plant <I>Curcuma longa</I>, is known to induce autophagy in various cancer cells, including lung cancer. In the present study, we also confirmed by LC3 immunofluorescence and immunoblotting analyses that curcumin triggers autophagy in the human lung adenocarcinoma A549 cell line. In parallel with autophagy induction, the gene expression of human GD3 synthase (hST8Sia I) responsible for ganglioside GD3 synthesis was markedly elevated in response to curcumin in the A549 cells. To investigate the transcriptional activation of hST8Sia I associated with the autophagy formation in curcumin-treated A549 cells, functional characterization of the 5′-flanking region of the hST8Sia I gene was carried out using the luciferase reporter assay system. Deletion analysis demonstrated that the -1146 to -646 region, which includes the putative c-Ets-1, CREB, AP-1, and NF-κB binding sites, functions as the curcumin-responsive promoter of hST8Sia I in A549 cells. The site-directed mutagenesis and chromatin immunoprecipitation assay demonstrated that the NF-κB binding site at -731 to -722 was indispensable for the curcumin-induced hST8Sia I gene expression in A549 cells. Moreover, the transcriptional activation of hST8Sia I by the curcumin A549 cells was strongly inhibited by compound C, an inhibitor of AMP-activated protein kinase (AMPK). These results suggest that curcumin controls hST8Sia I gene expression via AMPK signal pathway in A549 cells.</P>
Ha, Sun-Hyung,Lee, Ji-Min,Kwon, Kyung-Min,Kwak, Choong-Hwan,Abekura, Fukushi,Park, Jun-Young,Cho, Seung-Hak,Lee, Kichoon,Chang, Young-Chae,Lee, Young-Choon,Choi, Hee-Jung,Chung, Tae-Wook,Ha, Ki-Tae,Ch MDPI 2016 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.17 No.5
<P>Gangliosides have been known to play a role in the regulation of apoptosis in cancer cells. This study has employed disialyl-ganglioside GD1b to apoptosis in human breast cancer MCF-7 cells using exogenous treatment of the cells with GD1b and endogenous expression of GD1b in MCF-7 cells. First, apoptosis in MCF-7 cells was observed after treatment of GD1b. Treatment of MCF-7 cells with GD1b reduced cell growth rates in a dose and time dependent manner during GD1b treatment, as determined by XTT assay. Among the various gangliosides, GD1b specifically induced apoptosis of the MCF-7 cells. Flow cytometry and immunofluorescence assays showed that GD1b specifically induces apoptosis in the MCF-7 cells with Annexin V binding for apoptotic actions in early stage and propidium iodide (PI) staining the nucleus of the MCF-7 cells. Treatment of MCF-7 cells with GD1b activated apoptotic molecules such as processed forms of caspase-8, -7 and PARP (Poly(ADP-ribose) polymerase), without any change in the expression of mitochondria-mediated apoptosis molecules such as Bax and Bcl-2. Second, to investigate the effect of endogenously produced GD1b on the regulation of cell function, UDP-gal: β1,3-galactosyltransferase-2 (GD1b synthase, Gal-T2) gene has been transfected into the MCF-7 cells. Using the GD1b synthase-transfectants, apoptosis-related signal proteins linked to phenotype changes were examined. Similar to the exogenous GD1b treatment, the cell growth of the GD1b synthase gene-transfectants was significantly suppressed compared with the vector-transfectant cell lines and transfection activated the apoptotic molecules such as processed forms of caspase-8, -7 and PARP, but not the levels of expression of Bax and Bcl-2. GD1b-induced apoptosis was blocked by caspase inhibitor, Z-VAD. Therefore, taken together, it was concluded that GD1b could play an important role in the regulation of breast cancer apoptosis.</P>
( Sun Hyung Ha ),( Ji Min Lee ),( Kyung Min Kwon ),( Choong Hwan Kwak ),( Fukushi Abekura ),( Jun Young Park ),( Seung Hak Cho ),( Kichoon Lee ),( Young Chae Chang ),( Young Choon Lee ),( Hee Jung Cho 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Gangliosides have been known to play a role in the regulation of apoptosis in cancer cells. This study has employed disialyl-ganglioside GDlb to apoptosis in human breast cancer MCF-7 cells using exogenous treatment of the cells with GDlb and endogenous expression of GDlb in MCF-7 cells. First, apoptosis in MCF-7 cells was observed after treatment of GDlb. Treatment of MCF-7 cells with GDlb reduced cell growth rates in a dose and time dependent manner during GDlb treatment, as determined by XTT assay. Among the various gangliosides, GDlb specifically induced apoptosis of the MCF-7 cells. Flow cytometry and immunofluorescence assays showed that GDlb specifically induces apoptosis in the MCF-7 cells with Annexin V binding for apoptotic actions in early stage and propidium iodide (PI) staining the nucleus of the MCF-7 cells. Treatment of MCF-7 cells with GDlb activated apoptotic molecules such as processed forms of caspase-S, -7 and PARP (Poly(ADP-ribose) polymerase), without any change in the expression of mitochondria-mediated apoptosis molecules such as Bax and Bcl-2. Second, to investigate the effect of endogenously produced GDlb on the regulation of cell function, UDP-gal: [β1,3-galactosyltransferase-2 (GDlb synthase, Gal-T2) gene has been transfected into the MCF-7 cells. Using the GDlb synthase-transfectants, apoptosis-related signal proteins linked to phenotype changes were examined. Similar to the exogenous GDlb treatment, the cell growth of the GDlb synthase gene-transfectants was significantly suppressed compared with the vector-transfectant cell lines and transfection activated the apoptotic molecules such as processed forms of caspase-S, -7 and PARP, but not the levels of expression of Bax and Bcl-2. GDlb-induced