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  • Title: The glycine analogue, aminomethanesulfonic acid, inhibits LPS-induced production of TNF-alpha in isolated rat Kupffer cells and exerts hepatoprotective effects in mice.
    Author: Ishizaki-Koizumi S, Sonaka I, Takei Y, Ikejima K, Sato N.
    Journal: Biochem Biophys Res Commun; 2004 Sep 17; 322(2):514-9. PubMed ID: 15325260.
    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.
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