Abstract:
:The activation of Kupffer cells represents a central mechanism of liver injury involving the production of TNF-alpha. It is known that glycine prevents LPS-induced production of TNF-alpha in isolated Kupffer cells. In this study, the possibility that glycine analogues might affect Kupffer cells was investigated. As a result, aminomethanesulfonic acid (AMS) inhibited the production of TNF-alpha in LPS-stimulated Kupffer cells. Furthermore, LPS treatment caused a transient increase in intracellular calcium ([Ca(2+)](i)) which was blunted by AMS. Thus, the addition of AMS is protective against the LPS-induced increase [Ca(2+)](i) and subsequent production of TNF-alpha. Moreover, in vivo studies demonstrated that pretreatment of mice with AMS increased the rate of survival after injection with LPS/d-gal and reduced the TNF-alpha serum level and the mRNA level in the liver. These results indicate that intake of AMS attenuates the LPS-induced hepatotoxicity resulting from activation of Kupffer cells.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Ishizaki-Koizumi S,Sonaka I,Takei Y,Ikejima K,Sato Ndoi
10.1016/j.bbrc.2004.07.147subject
Has Abstractpub_date
2004-09-17 00:00:00pages
514-9issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(04)01646-8journal_volume
322pub_type
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