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首页> 外文期刊>Life sciences >Synthetic triglyceride containing an arachidonic acid branch (8A8) prevents lipopolysaccharide-induced liver injury.
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Synthetic triglyceride containing an arachidonic acid branch (8A8) prevents lipopolysaccharide-induced liver injury.

机译：含有花生四烯酸分支（8A8）的合成甘油三酸酯可防止脂多糖诱导的肝损伤。

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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).
机译：目的：在这项研究中，我们研究了含有花生四烯酸分支（8A8）的甘油三酸酯对脂多糖（LPS）诱导的巨噬细胞中肿瘤坏死因子（TNF）-α和一氧化氮（NO）产生的影响，以及LPS-引起大鼠肝损伤。主要方法：RAW264.7巨噬细胞与8A8和LPS（100ng / ml）共同孵育，并检测TNF-αmRNA /蛋白质水平，核因子（NF）-κBDNA结合活性，诱导型NO合酶（NOS2）的表达。 ），并测量NO（2）的产生。在静脉注射LPS（5mg / kg）之前，给雄性Wistar大鼠单次腹膜内注射8A8，然后评估肝脏组织学，凋亡细胞死亡，血清TNF-α水平和肝TNF-αmRNA。主要发现：8A8以剂量依赖的方式抑制了LPS诱导的RAW264.7巨噬细胞TNF-α产生的增加，在100ppm时抑制40％。此外，在RAW264.7巨噬细胞中，8A8剂量依赖性地防止了LPS诱导的TNF-αmRNA水平以及NF-κBDNA结合活性的增加。从这些细胞中释放的LPS诱导的NOS2和NO（2）的释放也以剂量依赖性方式被8A8降低。在体内，在LPS之前30分钟给予8A8（100microl / kg），可很大程度上防止LPS诱导的肝损伤，包括肝细胞凋亡。确实，8A8使血清TNF-α和肝TNF-αmRNA水平的升高明显减弱。意义：8A8可能通过抑制肝巨噬细胞产生的TNF-α和NO来预防LPS诱导的肝损伤，这表明8A8作为免疫调节营养物可用于预防/治疗内毒素相关的器官损伤，包括酒精性肝病和非酒精性脂肪性肝炎（NASH）。

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