TY - JOUR
T1 - Protective effect of linoleic acid on IFN γ-induced cellular injury in primary culture hepatocytes
AU - Liang, Jun Feng
AU - Akaike, Toshihiro
PY - 1998/2
Y1 - 1998/2
N2 - We have previously demonstrated that treatment of hepatocytes with IFN γ results a series of cellular injury processes, including DNA synthesis arrest, membrane breakage and apoptosis. In the present work, we show that IFN γ suppresses cellular respiration and protein synthesis in hepatocytes, and that cellular respiration suppression is an early event in the IFN γ-induced cellular injuries. Polyunsaturated fatty acids (PUFAs) increased cellular respiration of hepatocytes, but only linoleic acid showed some protective effect against IFN γ-induced cellular respiration suppression. Linoleic acid also reduced other IFN γ-mediated cellular injuries, including membrane breakage and protein synthesis inhibition. Like linoleic acid, fetal bovine serum also inhibited IFN γ-induced cellular damage. Increased NAD levels were found in both IFN γ-treated and non-treated hepatocytes following the addition of PUFAs, but clofibrate, a peroxisome proliferator, bromophenacyl bromide (BPB), an inhibitor of phospholipase, nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase, and arachidonic acid, a metabolite of linoleic acid, did not inhibit IFN γ-induced cellular injury. In addition, the combination of linoleic acid and IFN γ induced nitric oxide (NO) synthesis in hepatocytes. These results suggest that fatty acid may play an important role in liver homeostasis during chronic inflammatory states and sepsis.
AB - We have previously demonstrated that treatment of hepatocytes with IFN γ results a series of cellular injury processes, including DNA synthesis arrest, membrane breakage and apoptosis. In the present work, we show that IFN γ suppresses cellular respiration and protein synthesis in hepatocytes, and that cellular respiration suppression is an early event in the IFN γ-induced cellular injuries. Polyunsaturated fatty acids (PUFAs) increased cellular respiration of hepatocytes, but only linoleic acid showed some protective effect against IFN γ-induced cellular respiration suppression. Linoleic acid also reduced other IFN γ-mediated cellular injuries, including membrane breakage and protein synthesis inhibition. Like linoleic acid, fetal bovine serum also inhibited IFN γ-induced cellular damage. Increased NAD levels were found in both IFN γ-treated and non-treated hepatocytes following the addition of PUFAs, but clofibrate, a peroxisome proliferator, bromophenacyl bromide (BPB), an inhibitor of phospholipase, nordihydroguaiaretic acid (NDGA), an inhibitor of lipoxygenase, and arachidonic acid, a metabolite of linoleic acid, did not inhibit IFN γ-induced cellular injury. In addition, the combination of linoleic acid and IFN γ induced nitric oxide (NO) synthesis in hepatocytes. These results suggest that fatty acid may play an important role in liver homeostasis during chronic inflammatory states and sepsis.
KW - Cellular injury
KW - Hepatocyte
KW - IFN γ
KW - Linoleic acid
KW - Nitric oxide
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U2 - 10.1093/oxfordjournals.jbchem.a021924
DO - 10.1093/oxfordjournals.jbchem.a021924
M3 - Article
C2 - 9538194
AN - SCOPUS:0031935109
SN - 0021-924X
VL - 123
SP - 213
EP - 218
JO - Journal of Biochemistry
JF - Journal of Biochemistry
IS - 2
ER -