Open AccessTNF‐α and heat‐shock protein gene expression in ischemic‐injured liver from fasted and non‐fasted rats. Role of donor fasting in the prevention of reperfusion injury following liver transplantation
Author(s) -
Nishihara M.,
Sumimoto R.,
Fukuda Y.,
Southard J. H.,
Asahara T.,
Kawaishi H.,
Dohi K.
Publication year - 1998
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/j.1432-2277.1998.tb01171.x
Subject(s) - medicine , transplantation , liver transplantation , heat shock protein , endocrinology , shock (circulatory) , glycogen , hsp70 , messenger rna , ischemia , reperfusion injury , gene expression , tumor necrosis factor alpha , andrology , gene , biology , biochemistry
We have previously shown that livers from long‐term‐fasted rats acquire tolerance to warm ischemic injury following transplantation, despite the fact that fasting depletes glycogen and ATP from the liver. The precise mechanism of the protective effect induced by donor fasting, however, is still a matter of controversy. In this experiment we determined heat‐shock protein (GRP78) mRNA expression in livers during long‐term fasting and TNF‐α mRNA expression in transplanted livers exposed to warm ischemia. We also measured the concentration of TNF‐α by ELISA in the ascitic fluid of fed and fasted rats injected intraperitoneally with zymosan to investigate why livers from fasted rats tolerate ischemic injury better. There seemed to be a positive correlation between GRP78 mRNA expression and survival. TNF‐α secretion into the ascitic fluid of fasted rats was markedly suppressed, and fasting donor animals induced cytoprotective substances, such as GRP78, in the liver. These factors may contribute to the tolerance to ischemic injury produced by donor fasting.