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18篇 您的检索式:作者名="Osamu Handa"
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1Partially hydrolyzed guar gum attenuates non-alcoholic fatty liver disease in mice through the gut-liver axis显示文摘BACKGROUND The gut-liver axis has attracted much interest in the context of chronic liver disease pathogenesis.Prebiotics such as dietary fibers were shown to attenuate non-alcoholic fatty liver disease(NAFLD)by modulating gut microbiota.Partially hydrolyzed guar gum(PHGG),a water-soluble dietary fiber,has been reported to alleviate the symptoms of various intestinal diseases and metabolic syndromes.However,its effects on NAFLD remain to be fully elucidated.To determine whether treatment with PHGG attenuates NAFLD development in mice through the gut-liver axis.METHODS Seven-week-old male C57BL/6J mice with increased intestinal permeability were fed a control or atherogenic(Ath)diet(a mouse model of NAFLD)for 8 wk,with or without 5%PHGG.Increased intestinal permeability was induced through chronic intermittent administration of low-dose dextran sulfate sodium.Body weight,liver weight,macroscopic findings in the liver,blood biochemistry[aspartate aminotransferase(AST)and alanine aminotransferase(ALT),total cholesterol,triglyceride,free fatty acids,and glucose levels],liver histology,myeloperoxidase activity in liver tissue,mRNA expression in the liver and intestine,serum endotoxin levels in the portal vein,intestinal permeability,and microbiota and short-chain fatty acid(SCFA)profiles in the cecal samples were investigated.RESULTS Mice with increased intestinal permeability subjected to the Ath diet showed significantly increased serum AST and ALT levels,liver fat accumulation,liver inflammatory(tumor necrosis factor-αand monocyte chemotactic protein-1)and fibrogenic(collagen 1a1 andαsmooth muscle actin)marker levels,and liver myeloperoxidase activity,which were significantly attenuated by PHGG treatment.Furthermore,the Ath diet combined with increased intestinal permeability resulted in elevated portal endotoxin levels and activated toll-like receptor(TLR)4 and TLR9 expression,confirming that intestinal permeability was significantly elevated,as observed by evaluating the lumen-to-blood clearance of fluorescein isothiocyanate-conjugated dextran.PHGG treatment did not affect fatty acid metabolism in the liver.However,it decreased lipopolysaccharide signaling through the gut-liver axis.In addition,it significantly increased the abundance of cecal Bacteroides and Clostridium subcluster XIVa.Treatment with PHGG markedly increased the levels of SCFAs,particularly,butyric acid,acetic acid,propionic acid,and formic acid,in the cecal samples.CONCLUSION PHGG partially prevented NAFLD development in mice through the gut-liver axis by modulating microbiota and downstream SCFA profiles.Shun Takayama Kazuhiro Katada Tomohisa Takagi Takaya Iida Tomohiro Ueda Katsura Mizushima Yasuki Higashimura Mayuko Morita Tetsuya Okayama Kazuhiro Kamada Kazuhiko Uchiyama Osamu Handa Takeshi Ishikawa Zenta Yasukawa Tsutomu Okubo Yoshito Itoh Yuji Naito 2021World Journal of Gastroenterology2021,27,18:4
2Rebamipide, a Gastroprotective Drug, Inhibits Indomethacin-Induced Apoptosis in Cultured Rat Gastric Mucosal Cells: Association with the Inhibition of Growth Arrest and DNA Damage-Induced 45α Expression显示文摘Yuji Naito Hirokazu Kajikawa Katsura Mizushima Makoto Shimozawa Masaaki Kuroda Kazuhiro Katada Tomohisa Takagi Osamu Handa Satoshi Kokura Hiroshi Ichikawa Norimasa Yoshida Hirofumi Matsui Toshikazu Yoshikawa 2005Digestive Diseases and Sciences2005,,1:2
3Therapy of Helicobacter pylori : Present Medley and Future Prospective显示文摘Amin Talebi Bezmin Abadi Osamu Handa 2014BioMed Research International2014,,:2
4Rosuvastatin reduces rat intestinal ischemia-reperfusion injury associated with the preservation of endothelial nitric oxide synthase protein显示文摘瞄准:为了在 ischemia-reperfusion (红外) 上调查 rosuvastatin 的保护的效果,并且在内皮的氮的氧化物 synthase (eNOS ) 的表示上决定这个代理人的效果,在老鼠导致了小肠的损害和发炎蛋白质。方法:肠的损坏被为 30 min 夹钳优异 mes 伤寒动脉和腹的箱子在男 Sprague-Dawley 老鼠导致,为 60 min 由灌注列在后面。在生理盐水溶解的 Rosuvastatin intraperitoneally 被管理在局部缺血前的 60 min。肠的粘膜损害和发炎的严厉被几个生物化学的标记,以及由组织检查所见评估。eNOS 的蛋白质层次被西方的污点决定。结果:当粘膜的索引损坏,管腔内血红素和蛋白质的层次显著地在假冒操作组与那些相比在红外组被增加。然而,这些增加被处理显著地以一种剂量依赖者方式与 rosuvastatin 禁止。rosuvastatin 的保护的效果被组织检查所见也证实。到红外的小肠的暴露导致了 thiobarbituric 的重要增加描绘的粘膜发炎酸反应的物质,联系织物的 myeloperoxidase 活动,和老鼠的粘膜内容导致 cytokine 的嗜中性的 chemoattractant-1 (CINC-1 ) 和肿瘤坏死 factor-alpha (TNF-alpha ) 。在红外以后的煽动性的参数的这些增加被预告的处理显著地在 10 mg/kg 的剂量与 rosuvastatin 禁止。而且, CINC-1 和 TNF-alpha 的 mRNA 表示在红外以后被增加,并且这增加被 rosuvastatin 也禁止。eNOS 的粘膜蛋白质层次在红外期间减少了,但是在与 rosuvastatin 对待的老鼠被保存。结论:Rosuvastatin 禁止老鼠红外导致的肠的损害和发炎,和它的保护与 eNOS 的保藏被联系蛋白质。Yuji Naito Kazuhiro Katada Tomohisa Takagi Hisato Tsuboi Masaaki Kuroda Osamu Handa Satoshi Kokura Norimasa Yoshida Hiroshi Ichikawa Toshikazu Yoshikawa 2006World Journal of Gastroenterology2006,12,13:2
5Diagnostic Methods of Helicobacter pylori Infection for Epidemiological Studies: Critical Importance of Indirect Test Validation显示文摘Muhammad Miftahussurur Yoshio Yamaoka Osamu Handa 2016BioMed Research International2016,,:1
6Multifaceted Assessment of Chronic Gastritis: A Study of Correlations between Serological, Endoscopic, and Histological Diagnostics显示文摘Toshitatsu Takao Takeshi Ishikawa Takashi Ando Madoka Takao Tsuguhiro Matsumoto Yutaka Isozaki Mika Okita Yasuyuki Nagao Hirokazu Oyamada Keiichi Yokoyama Atsushi Tatebe Kazuhiko Uchiyama Osamu Handa Tomohisa Takagi Nobuaki Yagi Satoshi Kokura Yuji Naito 2011Gastroenterology Research and Practice2011,,:1
7Anoxia/reoxygenation induces epithelial-mesenchymal transition in humancolon cancer cell lines显示文摘Manabu Okajima Satoshi Kokura Takeshi Ishikawa Katsura Mizushima Reiko Tsuchiya Tatsuzo Matsuyama Satoko Adachi Tetsuya Okayama Naoyuki Sakamoto Kazuhiro Kamada Kazuhiro Katada Kazuhiko Uchiyama Osamu Handa Tomohisa Takagi Nobuaki Yagi Yuji Naito Toshikaz 2013Oncology Reports2013,,:1
8CagA protein of Helicobacter pylori : A hijacker of gastric epithelial cell signaling显示文摘Osamu Handa Yuji Naito Toshikazu Yoshikawa 2006Biochemical Pharmacology2006,,11:1
9Heat-shock protein 27 (Hsp27) as a target of methylglyoxal in gastrointestinal cancer显示文摘Tomoko Oya-Ito Yuji Naito Tomohisa Takagi Osamu Handa Hirofumi Matsui Masaki Yamada Keisuke Shima Toshikazu Yoshikawa 2011BBA - Molecular Basis of Disease2011,,7:1
10Helicobacter pylori: a ROS-inducing bacterial species in the stomach显示文摘Osamu Handa Yuji Naito Toshikazu Yoshikawa 2010Inflammation Research2010,,12:1
11Endoscopic diagnosis of small intestinal diseases显示文摘Osamu Handa Yuji Naito Tetsuya Okayama Naohisa Yoshida Kazuhiro Kamada Kazuhiro Katada Kazuhiko Uchiyama Takeshi Ishikawa Tomohisa Takagi Hideyuki Konishi Nobuaki Yagi Satoshi Kokura Toshikazu Yoshikawa 2013Clinical Journal of Gastroenterology2013,,2:1
12The detection of surface patterns by flexible spectral imaging color enhancement without magnification for diagnosis of colorectal polyps显示文摘Naohisa Yoshida Yuji Naito Yutaka Inada Munehiro Kugai Ken Inoue Kazuhiko Uchiyama Osamu Handa Tomohisa Takagi Hideyuki Konishi Nobuaki Yagi Yasutaka Morimoto Naoki Wakabayashi Akio Yanagisawa Toshikazu Yoshikawa 2012International Journal of Colorectal Disease2012,,5:1
13Helicobacter pylori: a ROS-inducing bacterial species in the stomach显示文摘Osamu Handa Yuji Naito Toshikazu Yoshikawa 2010Inflammation Research2010,,12:1
14Phase II trial of combined regional hyperthermia and gemcitabine for locally advanced or metastatic pancreatic cancer显示文摘Takeshi Ishikawa Satoshi Kokura Naoyuki Sakamoto Takashi Ando Eiko Imamoto Takeshi Hattori Hirokazu Oyamada Naomi Yoshinami Masafumi Sakamoto Kazutomo Kitagawa Yoko Okumura Naohisa Yoshida Kazuhiro Kamada Kazuhiro Katada Kazuhiko Uchiyama Osamu Handa Tomo 2012International Journal of Hyperthermia2012,,7:1
15Effect of hyperthermia combined with gemcitabine on apoptotic cell death in cultured human pancreatic cancer cell lines显示文摘Satoko Adachi Satoshi Kokura Tetsuya Okayama Takeshi Ishikawa Tomohisa Takagi Osamu Handa Yuji Naito Toshikazu Yoshikawa 2009International Journal of Hyperthermia2009,,3:1
16Helicobacter pylori : a ROS-inducing bacterial species in the stomach显示文摘Osamu Handa Yuji Naito Toshikazu Yoshikawa 2010Inflammation Research2010,,12:1
17Involvement of reactive oxygen species in indomethacin-induced apoptosis of small intestinal epithelial cells显示文摘Tatsushi Omatsu Yuji Naito Osamu Handa Natsuko Hayashi Katsura Mizushima Ying Qin Ikuhiro Hirata Satoko Adachi Tetsuya Okayama Etsuko Kishimoto Tomohisa Takagi Satoshi Kokura Hiroshi Ichikawa Toshikazu Yoshikawa 2009Journal of Gastroenterology2009,,19:1
18Rebamipide promotes healing of colonic ulceration through enhanced epithelial restitution显示文摘AIM:To investigate the efficacy of rebamipide in a rat model of colitis and restitution of intestinal epithelial cells in vitro.METHODS:Acute colitis was induced with trinitrobenzene sulfonic acid(TNBS)in male Wistar rats.Rats received intrarectal rebamipide treatment daily starting on day 7 and were sacrificed on day 14 after TNBS administration.The distal colon was removed to evaluate the various parameters of inflammation.Moreover,wound healing assays were used to determine the enhanced restitution of rat intestinal epithelial(RIE)cells treated with rebamipide.RESULTS:Intracolonic administration of rebamipide accelerated TNBSinduced ulcer healing.Increases in the wet weight of the colon after TNBS administration were significantly inhibited by rebamipide.The wound assay revealed that rebamipide enhanced the migration of RIE cells through phosphorylation of extracellular signalregulated kinase(ERK)and activation of Rho kinase.CONCLUSION:Rebamipide enema healed intestinal injury by enhancing restitution of RIE cells,via ERK activation.Rebamipide might be a novel therapeutic approach for inflammatory bowel disease.Tomohisa Takagi Yuji Naito Kazuhiko Uchiyama Toshimitsu Okuda Katsura Mizushima Takahiro Suzuki Osamu Handa Takeshi Ishikawa Nobuaki Yagi Satoshi Kokura Hiroshi Ichikawa Toshikazu Yoshikawa 2011World Journal of Gastroenterology2011,17,33:0
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