Effect of inducible nitric oxide synthase on apoptosis in Candida-induced acute lung injury
-
- Hosogi Shigekuni
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Iwasaki Yoshinobu
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Yamada Takahiro
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Komatani-Tamiya Nobuyo
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Hiramatsu Atsushi
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Kohno Yoshihito
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Ueda Mikio
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Arimoto Taichiro
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
-
- Marunaka Yoshinori
- Department of Respiratory Medicine, Graduate School of Medical Science, Kyoto Prefectural University of Medicine Department of Molecular Cell Physiology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine
この論文をさがす
抄録
Excessive nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) aggravates acute lung injury (ALI) by producing peroxinitrite. We previously showed that the expression of iNOS and lung injury were suppressed by inhalation of a novel iNOS inhibitor, ONO-1714, in mice with Candida-induced ALI, and that nitric oxide produced by iNOS and apoptosis of epithelial cells were found to have a crucial role in Candida-induced ALI. In the present study, we investigated the effect of NO on the apoptosis of alveolar epithelial cells in Candida-induced ALI. Mice were pretreated by inhalation of ONO-1714 or saline (vehicle control of ONO-1714), and were given an intravenous injection of Candida albicans to induce ALI. After 24 h from injection of Candida albicans, we performed bronchoalveolar lavage and removed lung tissues. We assessed apoptosis on the basis of TUNEL staining and caspase 3 activity. Our results showed that apoptosis was suppressed by inhibition of iNOS-derived NO production by ONO-1714 inhalation. The augmented production of NO increased FasL, TNF-α, and mRNA production of Bax of lung that induced apoptosis of alveolar epithelial cells. Inhibition of iNOS-derived NO production by ONO-1714 inhalation ameliorated Candida-induced ALI and improved survival by suppressing apoptosis of alveolar epithelial cells.
収録刊行物
-
- Biomedical Research
-
Biomedical Research 29 (5), 257-266, 2008
バイオメディカルリサーチプレス
- Tweet
詳細情報 詳細情報について
-
- CRID
- 1390001204901331456
-
- NII論文ID
- 130004470724
-
- ISSN
- 1880313X
- 03886107
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- Crossref
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可