Selectively Induced Apoptosis in Human Neutrophils in the Presence of Oxidative Phenoxazines, 2-Amino-4,4α-dihydryo-4α-7H-phenoxazine-3-one and 2-Aminophenoxazine-3-one, Preceded by Decrease of Intracellular pH, Depolarization of the Mitochondria, and Inh

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概要

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• The present research investigated the effect of the oxidative phenoxazines, 2-amino-4,4α-dihydryo-4α-7H-phenoxazine-3-one (Phx-1) and 2-amino-phenoxazine-3-one (Phx-3) on apoptosis induction and apoptosis-related early events in human neutrophils. When Phx-1 or Phx-3 was administered to freshly drawn human blood for 18 h, these phenoxazines caused apoptotic cell death morphologically characterized by condensation of the nucleus in neutrophils, without causing it in lymphocytes and monocytes. Apoptosis, which was detectable by microscopic analysis and by using flow-cytometry, occurred significantly in human neutrophils isolated from freshly drawn blood, 6 h after the administration of 50 μM Phx-1 and Phx-3. After 24 h, every isolated neutrophil treated with Phx-1 or Phx-3 fell into apoptosis or lost its morphology, while many of the neutrophils without these phenoxazines remained alive, with normal morphology. Apoptosis-related early events including a decrease in intracellular pH (pHi) and depolarization of the mitochondria occurred in the isolated neutrophils, 30 min and 6 h after the administration of Phx-1 or Phx-3, respectively. Superoxide generation from the isolated neutrophils mimicked by phorbol myristate acetate (PMA) was very markedly inhibited by 100 μM Phx-1 or Phx-3. This result could be explained, in part, by the fact that the insufficient supply of NADPH (nicotinamide adenine dinucleotide phosphate, reduced form) was caused by pHi decrease in neutrophils treated with Phx-1 or Phx, because NADPH is necessary for NADPH oxidase responsible for generating superoxide in the cells. The present results suggest that Phx-1 and Phx-3 have the capacity of selectively inducing apoptosis in human neutrophils and that these phenoxazines may be useful as specific drugs to induce apoptotic cell death of human neutrophils and thereby prevent inflammation caused by these phagocytic cells.

• 社団法人 日本薬理学会の論文
• 2011-11-20

著者

• Che Xiao-fang

  Department Of Molecular Oncology Graduate School Of Medicine Kagoshima University

• Che Xiao-fang

  Department Of Cancer Chemotherapy Institute For Cancer Research Kagoshima University

• Tomoda Akio

  Dep. Of Biochemistry Tokyo Medical Univ. Jpn

• Tomoda Akio

  Department Of Biochemistry And Intractable Tokyo Medical University

• Tomoda Akio

  Department Of Biochemistry And Intractable Immune System Disease Research Center Tokyo Medical Unive

• Sumimoto Hideki

  Department Of Biochemistry Kyushu University School Of Medicine

• TABUCHI TAKANOBU

  Fourth Department of Surgery, Tokyo Medical University Ibaraki Medical Center

• Tabuchi Takafumi

  Fourth Department Of Surgery Tokyo Medical University Ibaraki Medical Center

• Miyazawa Keisuke

  Department Of Biochemistry And Intractable Immune System Disease Research Center Tokyo Medical Unive

• Adachi Masakazu

  AdaBio Co., Ltd., Japan

• Miyano Kei

  Department of Biochemistry, Kyushu University Graduate School of Medical Sciences, Japan

• Hiraishi Katsuya

  Adabio Co. Ltd.

• Miyazawa Keisuke

  Department Of Biochemistry Kyushu University Graduate School Of Medical Sciences

• Sumimoto Hideki

  Department Of Biochemistry Kyushu University Graduate School Of Medical Sciences

• Adachi Masakazu

  Adabio Co. Ltd.

• Che Xiao-fang

  Department Of Biochemistry Tokyo Medical University

• Tabuchi Takanobu

  Fourth Department of Surgery, Tokyo Medical University, Ibaraki Medical Center

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