Biochemical and Biophysical Research Communications
Inhalation of hydrogen gas suppresses hepatic injury caused by ischemia/reperfusion through reducing oxidative stress
Section snippets
Materials and methods
Animals. Male C57 BL/6N mice (4 to 5 weeks old, 15–18 g) were purchased from Seac Yoshitomi, Ltd. (Yoshitomi-cho, Fukuoka, Japan). The mice were maintained under the standard conditions with a 12-h light/dark cycle, and permitted ad libitum access to standard rodent chow and tap water. The experiments were conducted according to the Guide for the Care and Use of Laboratory Animals and approved by the Animal Care and Use Committee of Nippon Medical School.
Liver I/R model. Mice underwent an I/R
Histopathological examination by HE staining
To investigate whether inhalation of hydrogen gas (H2) protects the liver against hepatic I/R injury, we histopathologically analyzed liver sections prepared from mice subjected to I/R with or without H2. When subjected to I/R insult without H2, profound degeneration was observed in the whole section and zonal cytoplasmic vacuolization preferentially developed in the centrilobular region (white areas in Fig. 1). Quantitative analysis using NIH Image software revealed that the degenerated area
Discussion
It has been reported that hepatic warm I/R injury consists of two phases [22], [23], [24], [25]. In the initial phase, Kupffer cells are activated by ischemia to produce reactive oxygen species (ROS) within 2 h after reperfusion, resulting in acute hepatocellular injury. The following late phase occurs 6 h after reperfusion, in which neutrophils, a well-known source of ROS [24], [26], [27], [28], [29], accumulate in the liver to more profoundly develop the hepatic damage. It is noted that reduced
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