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680 results on '"Matsui, Hirofumi"'

59. RGM1, a Cell Line Derived from Normal Gastric Mucosa of Rat

Author

Kobayashi, Ichizo, Kawano, Sunao, Tsuji, Shingo, Matsui, Hirofumi, Nakama, Akihiro, Sawaoka, Hitoshi, Masuda, Eiji, Takei, Yoshiyuki, Nagano, Kouichi, Fusamoto, Hideyuki, Ohno, Tadao, Fukutomi, Hisayuki, and Kamada, Takenobu

Published
1996

76. Mitochondria as Source of Free Radicals

Author

Majima, Hideyuki J., primary, Indo, Hiroko P., additional, Suenaga, Shigeaki, additional, Kaneko, Tsuyoshi, additional, Matsui, Hirofumi, additional, Yen, Hsiu Chuan, additional, and Ozawa, Toshihiko, additional

Published
2010
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81. Ammonia-induced apoptosis is accelerated at higher pH in gastric surface mucous cells

Author

Suzuki, Hideo, Yanaka, Akinori, Shibahara, Takeshi, Matsui, Hirofumi, Nakahara, Akira, Tanaka, Naomi, Muto, Hiroshi, Momoi, Takashi, and Uchiyama, Yasuo

Subjects
Helicobacter pylori, Ammonia -- Physiological aspects, Epithelial cells -- Physiological aspects, Gastric mucosa -- Physiological aspects, Biological sciences
Abstract

Gastric luminal ammonia produced by Helicobacter pylori has been shown to cause gastric mucosal injury. This study was conducted to examine the mechanisms by which gastric luminal ammonia causes apoptosis of gastric epithelial cells. Monolayers of GSM06 cells, developed from murine gastric surface mucous cells, were cultured in the absence or presence of 10-30 mM [NH.sub.4]Cl at ambient pH of 5.0, 6.0, and 7.0. In the presence of luminal [NH.sub.4]Cl, GSM06 cells showed 1) cell shrinkage and nuclear chromatin condensation, 2) DNA fragmentation into oligonucleosomes, 3) leakage of cytochrome c into cytosolic fraction without affecting bax expression, and 4) increases in activity of caspases-3 and -9. These changes were accentuated when the cells were cultured at pH 7.0. In the absence of [NH.sub.4]Cl, none of these changes was detected at any pH examined. These results suggest that gastric luminal ammonia, at concentrations detected in H. pylori-infected subjects, induces apoptosis of gastric epithelial cells by release of cytochrome c from mitochondria, followed by activation of caspases-9 and -3, especially at higher ambient pH. Helicobacter pylori; gastric epithelial cells

Published
2002

82. EGF promotes gastric mucosal restitution by activating [Na.sup.+]/[H.sup.+] exchange of epithelial cells

Author

Yanaka, Akinori, Suzuki, Hideo, Shibahara, Takeshi, Matsui, Hirofumi, Nakahara, Akira, and Tanaka, Naomi

Subjects
Epidermal growth factor -- Receptors, Gastric mucosa -- Physiological aspects, Biological sciences
Abstract

This study was conducted to determine whether the contributions of epidermal growth factor (EGF) to gastric mucosal restitution after injury are mediated by stimulation of [Na.sup.+]/[H.sup.+] exchangers in surface mucous cells (SMC). Intact sheets of guinea pig gastric mucosae were incubated in vitro. Intracellular pH (p[H.sub.i]) in SMC was measured fluorometrically, using 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein. Restitution after Triton X-100-induced injury was evaluated by recovery of electrical resistance. At neutral luminal pH, exogenous EGF (ex-EGF) increased p[H.sub.i] and enhanced restitution in the absence but not in the presence of serosal HC[O.sup.-.sub.3]. During exposure to luminal acid, ex-EGF not only prevented intracellular acidosis but also promoted restitution. These effects of ex-EGF were blocked by serosal amiloride or anti-EGF-receptor antibody. In the absence of ex-EGF, restitution was inhibited by replacement of luminal and serosal solutions with fresh solutions and was blocked more completely by serosal anti-EGF-receptor antibody. These results suggest that both endogenous and ex-EGF contribute to restitution via basolateral EGF receptors, with effects mediated, at least in part, by stimulation of basolateral [Na.sup.+]/[H.sup.+] exchangers. epidermal growth factor receptor; electrical resistance; [sup.3]H-labeled mannitol flux; intracellular pH; luminal acid

Published
2002

86. Antioxidant nanomedicine with cytoplasmic distribution in neuronal cells shows superior neurovascular protection properties

Author

Mujagić, Arnela, primary, Marushima, Aiki, additional, Nagasaki, Yukio, additional, Hosoo, Hisayuki, additional, Hirayama, Aki, additional, Puentes, Sandra, additional, Takahashi, Toshihide, additional, Tsurushima, Hideo, additional, Suzuki, Kensuke, additional, Matsui, Hirofumi, additional, Ishikawa, Eiichi, additional, Matsumaru, Yuji, additional, and Matsumura, Akira, additional

Published
2020
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96. Anticancer effect of linalool via cancer-specific hydroxyl radical generation in human colon cancer

Author

Villareal, Myra Orlina, Iwasaki, Kenichi, Zheng, Yun-Wen, Murata, Soichiro, Ito, Hiromu, Nakayama, Ken, Kurokawa, Tomohiro, Sano, Naoki, Nowatari, Takeshi, Villareal, Myra O, Nagano, Yumiko N, Isoda, Hiroko, Matsui, Hirofumi, and Ohkohchi, Nobuhiro

Abstract

AIM To investigate the anticancer mechanisms of the monoterpenoid alcohol linalool in human colon cancer cells. METHODS The cytotoxic effect of linalool on the human colon cancer cell lines and a human fibroblast cell line was examined using the WST-8 assay. The apoptosis-inducing effect of linalool was measured using the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay and flow cytometry with Annexin V. Oxidative stress was investigated by staining for diphenyl-1-pyrenylphosphine, which is a cellular lipid peroxidation marker, and electron spin resonance spectroscopy. Sixteen SCID mice xenografted with human cancer cells were randomized into 3 groups for in vivo analysis: control and low-dose and high-dose linalool groups. The control group was administered tap water orally every 3 d. The linalool treatment groups were administered 100 or 200 μg/kg linalool solution orally for the same period. All mice were sacrificed under anesthesia 21 d after tumor inoculation, and tumors and organs were collected for immunohistochemistry using an anti-4-hydroxynonenal antibody. Tumor weights were measured and compared between groups. RESULTS Linalool induced apoptosis of cancer cells in vitro, following the cancer-specific induction of oxidative stress, which was measured based on spontaneous hydroxyl radical production and delayed lipid peroxidation. Mice in the high-dose linalool group exhibited a 55% reduction in mean xenograft tumor weight compared with mice in the control group (P < 0.05). In addition, tumor-specific lipid peroxidation was observed in the in vivo model. CONCLUSION Linalool exhibited an anticancer effect via cancer-specific oxidative stress, and this agent has potential for application in colon cancer therapy.

Published
2016

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