TY - JOUR
T1 - Astilbin selectively induces dysfunction of liver-infiltrating cells - Novel protection from liver damage
AU - Xu, Qiang
AU - Wu, Feihua
AU - Cao, Jingsong
AU - Chen, Ting
AU - Jiang, Jieyun
AU - Saiki, Ikuo
AU - Koda, Akihide
PY - 1999/7/14
Y1 - 1999/7/14
N2 - The present study aimed to examine the effect of astilbin, a flavanoid, on liver injury. When administered during the effector but not induction phase, astilbin significantly decreased the liver injury induced by delayed-type hypersensitivity to picryl chloride in mice. The pretreatment of nonparenchymal cells but not hepatocytes with astilbin in vitro caused a concentration- and time-dependent inhibition against the damage. Nonparenchymal cells isolated from astilbin-administered mice also showed a significant incompetence of hepatotoxicity, correlated with the inhibition of serum transaminase elevation. However, astilbin did not protect from CCl 4-induced liver damage. Furthermore, the flavanoid markedly promoted the apoptosis of nonparenchymal cells from liver-injured mice, whereas did not influence those from naive mice. These results suggest that astilbin provides improvement against liver injury through a selective dysfunction of liver-infiltrating cells rather than by protecting the hepatocyte membrane. Such characteristics will be of significance to pave a new way for treating immunologically related liver diseases and for developing new drugs. Copyright (C) 1999 Elsevier Science B.V.
AB - The present study aimed to examine the effect of astilbin, a flavanoid, on liver injury. When administered during the effector but not induction phase, astilbin significantly decreased the liver injury induced by delayed-type hypersensitivity to picryl chloride in mice. The pretreatment of nonparenchymal cells but not hepatocytes with astilbin in vitro caused a concentration- and time-dependent inhibition against the damage. Nonparenchymal cells isolated from astilbin-administered mice also showed a significant incompetence of hepatotoxicity, correlated with the inhibition of serum transaminase elevation. However, astilbin did not protect from CCl 4-induced liver damage. Furthermore, the flavanoid markedly promoted the apoptosis of nonparenchymal cells from liver-injured mice, whereas did not influence those from naive mice. These results suggest that astilbin provides improvement against liver injury through a selective dysfunction of liver-infiltrating cells rather than by protecting the hepatocyte membrane. Such characteristics will be of significance to pave a new way for treating immunologically related liver diseases and for developing new drugs. Copyright (C) 1999 Elsevier Science B.V.
KW - Apoptosis
KW - Astilbin
KW - Delayed-type hypersensitivity
KW - Hepatoprotection
KW - Liver injury
KW - Picryl chloride
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U2 - 10.1016/S0014-2999(99)00401-X
DO - 10.1016/S0014-2999(99)00401-X
M3 - Article
C2 - 10448932
AN - SCOPUS:0033035926
SN - 0014-2999
VL - 377
SP - 93
EP - 100
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 1
ER -