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- 저자 : Takuya Matsuda (검색결과 4 건)
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Anti-cancer effects of enzyme-digested fucoidan extract from seaweed Mozuku
Teruya, Kiichiro,Matsuda, Sakiko,Nakano, Ayumi,Nishimoto, Takuya,Ueno, Masashi,Niho, Akitono,Yamashita, Makiko,Eto, Hiroshi,Katakura, Yoshinori,Shirahata, Sanetaka Institute of Agricultural Science 2009 Korean Journal of Agricultural Science Vol.36 No.1
Fucoidan is a uniquely-structured sulfated fucose-rich polysaccharide derived from brown algae. Recently, the abalone glycosidase-digested fucoidan extract (fucoidan extract) derived from seaweed Cladosiphon novae-caledoniae Kylin (Mozuku) draws much attention because of its clinical anti-cancer effect in Japan. Here, we report the cancer cells-specific apoptosis inducing effects of the fucoidan extract. The fucoidan extract suppressed the growth of various anchorage-dependent and -independent cancer cells. The fucoidan extract contained low molecular weight components, which induced apoptosis of human leukemic HL 60 cells but not of human lymphocytes. It was shown that the fucoidan extract lead caspase 3/7 activation and loss of mitochondrial membrane potential in HL 60 cells. Another function of the fucoidan extract was also observed. It has been known that sugar chain expression on the surface of cancer cell membrane changes dependent on their malignancy. The analysis on sugar chain expression profiling using FITC-labeled lectins revealed that the expression of concanavalin A (Con A) binding sugar chain was enhanced by the treatment of human lung adenocarcinoma A549, human uterine carcinoma HeLa and human fibrosarcoma HT1080 cells with the fucoidan extract. Con A-induced apoptosis of cancer cells was stimulated in a dose-and time-dependent manner by the treatment with the fucoidan extract but not of human normal fibroblast TIG-1 cells.
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Anti-cancer effects of enzyme-digested fucoidan extract from seaweed Mozuku
Kiichiro Teruya,Sakiko Matsuda,Ayumi Nakano,Takuya Nishimoto,Masashi Ueno,Akitono Niho,Makiko Yamashita,Hiroshi Eto,Yoshinori Katakura,Sanetaka Shirahata 충남대학교 농업과학연구소 2009 농업과학연구 Vol.36 No.1
Fucoidan is a uniquely-structured sulfated fucose-rich polysaccharide derived from brown algae. Recently, the abalone glycosidase-digested fucoidan extract (fucoidan extract) derived from seaweed Cladosiphon novae-caledoniae Kylin (Mozuku) draws much attention because of its clinical anti-cancer effect in Japan. Here, we report the cancer cells-specific apoptosis inducing effects of the fucoidan extract. The fucoidan extract suppressed the growth of various anchorage-dependent and -independent cancer cells. The fucoidan extract contained low molecular weight components, which induced apoptosis of human leukemic HL 60 cells but not of human lymphocytes. It was shown that the fucoidan extract lead caspase 3/7 activation and loss of mitochondrial membrane potential in HL 60 cells. Another function of the fucoidan extract was also observed. It has been known that sugar chain expression on the surface of cancer cell membrane changes dependent on their malignancy. The analysis on sugar chain expression profiling using FITC-labeled lectins revealed that the expression of concanavalin A (Con A) binding sugar chain was enhanced by the treatment of human lung adenocarcinoma A549, human uterine carcinoma HeLa and human fibrosarcoma HT1080 cells with the fucoidan extract. Con A-induced apoptosis of cancer cells was stimulated in a dose-and time-dependent manner by the treatment with the fucoidan extract but not of human normal fibroblast TIG-1 cells.
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Nguyen Thi Trang,Takuya Hirai,Tsukasa Yamamoto,Mari Matsuda,Naoko Okumura,Nguyen Thi Huong Giang,Nguyen Thi Lan,Ryoji Yamaguchi 대한수의학회 2014 JOURNAL OF VETERINARY SCIENCE Vol.15 No.3
The objectives of the present study were to evaluate theanatomic localization of porcine reproductive andrespiratory syndrome virus (PRRSV) in naturally infectedpigs and to determine whether oral fluid could be used todetect the virus in infected animals. Two sows, seven2-month-old grower pigs, and 70 6-month-old gilts wereincluded in this study. PRRSV in sera and oral fluid wereidentified by nested reverse transcription PCR (nRT-PCR)while lung, tonsil, and tissue associated with oral cavity weresubjected to nRT-PCR, immunohistochemistry, and in situhybridization. In sows, PRRSV was identified in oral fluidand tonsils. PRRSV was also detected in oral fluid, tonsils,salivary glands, oral mucosa, and lungs of all seven growerpigs. However, viremia was observed in only two growerpigs. Double staining revealed that PRRSV was distributedin macrophages within and adjacent to the tonsillar cryptepithelium. In gilts, the North American type PRRSV fieldstrain was detected 3 to 8 weeks after introducing theseanimals onto the farm. These results confirm previousfindings that PRRSV primarily replicates in tonsils and isthen shed into oral fluid. Therefore, oral fluid sampling maybe effective for the surveillance of PRRSV in breeding herds.
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Masanobu Tsubaki,Tomoya Takeda,Takuya Matsuda,Akihiro Kimura,Remi Tanaka,Sakiko Nagayoshi,Tadafumi Hoshida,Kazufumi Tanabe,Shozo Nishida 생화학분자생물학회 2023 BMB Reports Vol.56 No.2
Chronic myeloid leukemia (CML) has a markedly improvedprognosis with the use of breakpoint cluster region-abelson 1(BCR-ABL1) tyrosine kinase inhibitors (BCR-ABL1 TKIs). However,approximately 40% of patients are resistant or intolerantto BCR-ABL1 TKIs. Hypoxia-inducible factor 1α (HIF-1α) is ahypoxia response factor that has been reported to be highlyexpressed in CML patients, making it a therapeutic target forBCR-ABL1 TKI-sensitive CML and BCR-ABL1 TKI-resistant CML. In this study, we examined whether HIF-1α inhibitors inducecell death in CML cells and BCR-ABL1 TKI-resistant CML cells. We found that echinomycin and PX-478 induced cell death inBCR-ABL1 TKIs sensitive and resistant CML cells at similar concentrationswhile the cell sensitivity was not affected with imatinibor dasatinib in BCR-ABL1 TKIs resistant CML cells. In addition,echinomycin and PX-478 inhibited the c-Jun N-terminalkinase (JNK), Akt, and extracellular-regulated protein kinase 1/2(ERK1/2) activation via suppression of BCR-ABL1 and Met expressionin BCR-ABL1 sensitive and resistant CML cells. Moreover,treatment with HIF-1α siRNA induced cell death by inhibitingBCR-ABL1 and Met expression and activation of JNK,Akt, and ERK1/2 in BCR-ABL1 TKIs sensitive and resistant CMLcells. These results indicated that HIF-1α regulates BCR-ABL andMet expression and is involved in cell survival in CML cells,suggesting that HIF-1α inhibitors induce cell death in BCR-ABL1TKIs sensitive and resistant CML cells and therefore HIF-1α inhibitorsare potential candidates for CML treatment.
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