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RISS 인기검색어
- 검색키워드
- 저자 : (Evangeline C . Amor) (검색결과 4 건)
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Acebedo, Alvin Resultay,Amor, Evangeline Cancio,Jacinto, Sonia Donaldo Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.2
Voacanga globosa (Blanco), a plant endemic to the Philippines, is traditionally used especially by indigenous people of Bataan in the treatment of ulcers, wounds and tumorous growths. This study aimed to provide scientific evidence to therapeutic properties by determining cytotoxic and pro-apoptotic activity of HPLC fractions from leaves on HCT116 human colon carcinoma and A549 human lung carcinoma cell lines. Ethanolic extraction was performed on V globosa leaves followed by hexane and ethyl acetate partitioning. Silica gel column chromatography and high performance liquid chromatography (HPLC) produced MP1, MP2 and MP3 fractions. Cytotoxic activity of the fractions was determined through MTT assay against the cancer cell lines HCT116 and A549 and the non-cancer AA8 Chinese hamster ovarian cell line. Pro-apoptotic activities of the most active fractions were further assessed through DAPI staining, TUNEL assay and JC-1 mitochondrial membrane potential assay with HCT116 cells. While the MPI fraction exerted no significant activity against all cell lines tested, MP2 and MP3 fractions demonstrated high toxicity against HCT116 and A549 cells. The MP3 fraction induced formation of apoptotic bodies, condensed DNA and other morphological changes consistent with apoptosis of HCT116 cells and TUNEL assay showed significant increase in DNA fragmentation over time. In these cells, the MP3 fraction also induced mitochondrial membrane destabilization, which is generally associated with the beginning of apoptosis. Phytochemical analysis demonstrated the presence only of saponins and terpenoids in the MP3 fraction. The results indicate that the MP3 fraction exerts cytotoxic activity on HCT116 cells via induction of apoptosis triggered by loss of mitochondrial membrane potential crucial for cell survival.
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Ko, Hyeonseok,Kim, Young‐,Joo,Amor, Evangeline C.,Lee, Jong Wha,Kim, Han‐,Cheon,Kim, Hee Ju,Yang, Hyun Ok Wiley Subscription Services, Inc., A Wiley Company 2011 Journal of cellular biochemistry Vol.112 No.9
<P><B>Abstract</B></P><P>Dimethyl cardamonin (2′,4′‐dihydroxy‐6′‐methoxy‐3′,5′‐dimethylchalcone; DMC) is a naturally occurring chalcone, and it is the major compound isolated from the leaves of <I>Syzygium samarangense</I> (Blume) Merr. & L.M. Perry (Myrtaceae). Experiments were conducted to determine the effects of DMC on cell proliferation, cell‐cycle distribution, and programmed cell death in cultures of human colorectal carcinoma HCT116 and LOVO cells. Results showed that DMC inhibited HCT116 and LOVO cell proliferation and induced G<SUB>2</SUB>/M cell cycle arrest, which was associated with the conversion of microtubule associated protein light chain 3 (LC3)‐I–LC3‐II, an autophagosome marker, and the incorporation of monodansylcadaverine (MDC), a marker for the acidic compartment of autolysosomes or acidic vesicular organelles. The treatment of HCT116 and LOVO cells using a combination of DMC with an autophagy inhibitor, such as 3‐methyladenine (3‐MA), beclin 1 siRNA, or atg5 siRNA, suppressed the effect of DMC‐mediated anti‐proliferation. These results imply that DMC can suppress colorectal carcinoma HCT116 and LOVO cell proliferation through a G<SUB>2</SUB>/M phase cell‐cycle delay, and can induce autophagy, the hallmark of Type II programmed cell death (PCD). Taken together, our results suggest that DMC may be an effective chemotherapeutic agent for HCT116 and LOVO colorectal carcinoma cells. J. Cell. Biochem. 112: 2471–2479, 2011. © 2011 Wiley‐Liss, Inc.</P>
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Kim, Young‐,Joo,Kim, Han‐,Cheon,Ko, Hyeonseok,Amor, Evangeline C.,Lee, Jong Wha,Yang, Hyun Ok Wiley Subscription Services, Inc., A Wiley Company 2011 Journal of cellular biochemistry Vol.112 No.2
<P><B>Abstract</B></P><P>We identified a chalcone, 2′,4′‐dihydroxy‐6′‐methoxy‐3′‐methylchalcone (stercurensin), as an active compound isolated from the leaves of <I>Syzygium samarangense</I>. In the present study, the anti‐inflammatory effects and underlying mechanisms of stercurensin were examined using lipopolysaccharide (LPS)‐stimulated RAW264.7 cells and mice. To determine the effects of stercurensin in vitro, inducible nitric oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2) expression were analyzed by RT‐PCR and immunoblotting. Nuclear factor‐κB (NF‐κB) activation and its upstream signaling cascades were also investigated using a dual‐luciferase reporter assay, electrophoretic mobility shift assay, immunoblotting, immunofluorescence, and immunoprecipitation. To verify the effects of stercurensin in vivo, the mRNA expression levels of iNOS and COX‐2 were evaluated in isolated mouse peritoneal macrophages by quantitative real‐time PCR, and the production of tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), and IL‐1β were assessed in serum samples from mice using a Luminex system. Pretreatment with stercurensin reduced LPS‐induced iNOS and COX‐2 expression, thereby inhibiting nitric oxide (NO) and prostaglandin E<SUB>2</SUB> production, respectively. In addition, an inhibitory effect of stercurensin on NF‐κB activation was shown by the recovery of LPS‐induced inhibitor of κB (I‐κB) degradation after blocking the transforming growth factor‐β‐activated kinase 1 (TAK1)/I‐κB kinase signaling pathway. In mouse models, stercurensin negatively regulated NF‐κB‐dependent pro‐inflammatory mediators and cytokines. These results demonstrate that stercurensin modulates NF‐κB‐dependent inflammatory pathways through the attenuation of TAK1–TAB1 complex formation. Our findings demonstrating the anti‐inflammatory effects of stercurensin in vitro and in vivo will aid in understanding the pharmacology and mode of action of stercurensin. J. Cell. Biochem. 112: 548–558, 2011. © 2010 Wiley‐Liss, Inc.</P>
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