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Suppression of indomethacin-induced apoptosis in the small intestine due to Bach1 deficiency.

Authors :
Harusato, Akihito
Naito, Yuji
Takagi, Tomohisa
Uchiyama, Kazuhiko
Mizushima, Katsura
Hirai, Yasuko
Yamada, Shinya
Tuji, Toshifumi
Yoriki, Hiroyuki
Horie, Ryusuke
Inoue, Ken
Fukumoto, Kohei
Handa, Osamu
Ishikawa, Takeshi
Kokura, Satoshi
Minamiyama, Yukiko
Ichikawa, Hiroshi
Muto, Akihiko
Igarashi, Kazuhiko
Yoshikawa, Toshikazu
Source :
Free Radical Research; Jun2011, Vol. 45 Issue 6, p717-727, 11p, 3 Color Photographs, 7 Graphs
Publication Year :
2011

Abstract

BTB and CNC homologue 1 (Bach1) is a transcriptional repressor of heme oxygenase-1 (HO-1). This study hypothesized that Bach1 plays an important role in the indomethacin-induced apoptosis in the case of small-intestinal mucosal injury. Eight-week-old male C57BL/6 (wild-type) and homozygous Bach1-deficient C57BL/6 mice were included in this study. Mucosal injuries induced by subcutaneously administering indomethacin were evaluated macroscopically, histologically and biochemically. Indomethacin-induced injuries were improved in Bach1-deficient mice. Immunohistochemistry showed an increase in the number of HO-1-positive cells, which were mainly F4/80 positive macrophages, in Bach1-deficient mice. Indomethacin administration increased the expression of HO-1 mRNA and protein in the small intestine in Bach1-deficient mice. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining showed that the extent of apoptosis was suppressed in Bach1-deficent mice. In conclusion, deficiency of the Bach1 gene inhibited apoptosis and thus suppressed mucosal injury, indicating that Bach1 is a novel therapeutic target for indomethacin-induced intestinal injury. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
10715762
Volume :
45
Issue :
6
Database :
Complementary Index
Journal :
Free Radical Research
Publication Type :
Academic Journal
Accession number :
60029576
Full Text :
https://doi.org/10.3109/10715762.2011.574287