| Literature DB >> 19194039 |
Tadayuki Ikeda1, Kazuki Abe, Noriyuki Kuroda, Yujiro Kida, Hideo Inoue, Kenjiro Wake, Mitsuhiko Morito, Tetsuji Sato.
Abstract
The inhibition of apoptosis by glycyrrhizin (GL) in hepatic injury induced by injection of lipopolysaccharide (LPS)/D-galactosamine (D-GalN) was examined in the present study. Morphological and biochemical analyses of LPS/D-GalN-induced mouse liver injury revealed that apoptosis occurred exclusively in injured hepatocytes of the centrilobular area. The degree of hepatic injury was associated with a substantial number of hepatocytes undergoing apoptosis. Transaminase levels were significantly increased at 6 to 8 h after the injection of LPS/D-GalN compared with controls. GL inhibited the elevation of serum transaminase levels when it was given to mice at 30 min before the administration of LPS/D-GalN. Morphological analyses using the TUNEL-method showed GL significantly reduced the number of TUNEL-labeled cells in acute hepatitis induced with LPS/D-GalN-treatment. Cells from the pericentral hepatic injury region were dissected out using a microdissection-method, and the DNA-ladder was clearly documented. Furthermore, results obtained through the TUNEL-method were confirmed with an oligonucleosome-bound DNA ELISA. From the current results, it seems reasonable to conclude that the protective role of GL in LPS/D-GalN-induced liver injury is performed through the inhibition of hepatic apoptosis.Entities:
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Year: 2008 PMID: 19194039 DOI: 10.1679/aohc.71.163
Source DB: PubMed Journal: Arch Histol Cytol ISSN: 0914-9465