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  • Title: Synthetic triglyceride containing an arachidonic acid branch (8A8) prevents lipopolysaccharide-induced liver injury.
    Author: Piao N, Ikejima K, Kon K, Aoyama T, Osada T, Takei Y, Sato N, Watanabe S.
    Journal: Life Sci; 2009 Oct 21; 85(17-18):617-24. PubMed ID: 19647752.
    Abstract:
    AIMS: In this study, we investigated the effect of synthetic triglyceride containing an arachidonic acid branch (8A8) on lipopolysaccharide (LPS)-induced production of tumor necrosis factor (TNF)-alpha and nitric oxide (NO) in macrophages, and LPS-induced liver injury in the rat. MAIN METHODS: RAW264.7 macrophages were co-incubated with 8A8 and LPS (100ng/ml), and TNF-alpha mRNA/protein levels, nuclear factor (NF)-kappaB DNA binding activity, expression of inducible-type NO synthase (NOS2), and NO(2) production were measured. Male Wistar rats were given a single intraperitoneal injection of 8A8 prior to an intravenous injection of LPS (5mg/kg), and liver histology, apoptotic cell death, serum TNF-alpha levels, and hepatic TNF-alpha mRNA were then evaluated. KEY FINDINGS: LPS-induced increases in TNF-alpha production in RAW264.7 macrophages were blunted by 8A8 in a dose-dependent manner, with 40% inhibition at 100ppm. Further, 8A8 dose-dependently prevented LPS-induced increases in TNF-alpha mRNA levels, as well as NF-kappaB DNA binding activities, in RAW264.7 macrophages. LPS-induction of NOS2 and NO(2) release from these cells was also decreased by 8A8 in a dose-dependent manner. In vivo, LPS-induced liver injury, including hepatocyte apoptosis, was largely prevented when 8A8 (100microl/kg) was given 30min prior to LPS. Indeed, 8A8 blunted increases in both serum TNF-alpha and hepatic TNF-alpha mRNA levels significantly. SIGNIFICANCE: LPS-induced liver injury was prevented by 8A8 most likely through the inhibition of TNF-alpha and NO production from hepatic macrophages, suggesting a potential usefulness of 8A8 as an immuno-modulating nutrient for prevention/treatment of endotoxin-related organ injuries including alcoholic liver disease and non-alcoholic steatohepatitis (NASH).
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