BackgroundAcetaminophen (APAP) overdose is one of the most common causes of acute liver failure in many countries. The aim of the study was to describe the profiling of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in the plasma and liver of Acetaminophen -induced liver injured mice.MethodsA time course study was carried out using C57BL/6 mice after intraperitoneal administration of 300 mg/kg Acetaminophen 1 h, 3 h, 6 h, 12 h and 24 h. A high-throughput liquid chromatography mass spectrometry (LC-MS) lipidomic method was utilized to detect phosphatidylcholine and phosphatidylethanolamine species in the plasma and liver. The expressions of phosphatidylcholine and phosphatidylethanolamine metabolism related genes in liver were detected by quantitative Reverse transcription polymerase chain reaction (qRT-PCR) and Western-blot.ResultsFollowing Acetaminophen treatment, the content of many PC and PE species in plasma increased from 1 h time point, peaked at 3 h or 6 h, and tended to return to baseline at 24 h time point. The relative contents of almost all PC species in liver decreased from 1 h, appeared to be lowest at 6 h, and then return to normality at 24 h, which might be partly explained by the suppression of phospholipases mRNA expressions and the induction of choline kinase (Chka) expression. Inconsistent with PC profile, the relative contents of many PE species in liver increased upon Acetaminophen treatment, which might be caused by the down-regulation of phosphatidylethanolamine N-methyltransferase (Pemt).ConclusionsAcetaminophen overdose induced dramatic change of many PC and PE species in plasma and liver, which might be caused by damaging hepatocytes and interfering the phospholipid metabolism in Acetaminophen -injured liver.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-017-0540-4) contains supplementary material, which is available to authorized users.

Circular RNAs have been found to be aberrantly expressed in tumors and their significance in tumorigenesis has been focused on. The role of circDYNC1H1 in hepatocellular carcinoma (HCC) pathogenesis and its relationship with miR‐140‐5p were explored. The expression of circDYNC1H1, miR‐140‐5p, and SULT2B1 in HCC tissues and cells was measured, and Pearson's analysis was used to analyze their expression correlation. 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide and Transwell assays were performed to determine cell proliferation and migration. Binding between circDYNC1H1 and miR‐140‐5p was evaluated with RNA pull‐down assay. A luciferase reporter assay was conducted to assess the interaction between circDYNC1H1 and miR‐140‐5p and between miR‐140‐5p and SULT2B1. circDYNC1H1 was highly expressed in HCC tissues (n = 20), and it was negatively associated with the expression of miR‐140‐5p but positively correlated with SULT2B1 messenger RNA expression. circDYNC1H1 was upregulated in cell lines of HCC. Interference of circDYNC1H1 suppressed cell proliferation and migration of HCC. circDYNC1H1 acted as a sponge of miR‐140‐5p. miR‐140‐5p controlled SULT2B1 expression by targeting its 3′‐untranslated region. circDYNC1H1 enhanced SULT2B1 expression via sponging miR‐140‐5p. Downregulation of circDYNC1H1 disturbed cell proliferation and migration of HCC through miR‐140‐5p/SULT2B1 pathway. Silencing of circDYNC1H1 delayed tumor growth in HCC mouse model. Acting like a sponge of miR‐140‐5p, silenced circDYNC1H1 downregulated SULT2B1 to restrain HCC cell proliferation and migration, which is adverse to HCC growth and progression.

Novel indole amide derivatives C1‐C10 were successfully synthesized and characterized by 1H NMR, 13C NMR, IR, MS, and elemental analysis, and their molecular formulas were C14H10N6O, C13H10N4O, C16H13N3O2, C19H14N2O2, C16H11N3OS, C15H13N3O, C12H9N5O, C16H10ClN3OS, C15H17N3O2, and C13H14N2O3, respectively. The primary biological activities of these compounds were evaluated in vitro by the DPPH assay, H2O2‐induced oxidative stress injury assay, and cytotoxicity assay. The results indicated that compounds C1, C2, C4, C7, and C9 exhibited DPPH·scavenging ability, while C3, C4, C5, and C8 showed potent growth‐inhibitory activities against various human tumor cells, including MDA‐MB‐231, Hela, A549, and HT29. Interestingly, compound C4 showed potent scavenging effects on the DPPH radical and possessed protective effect on H2O2‐induced oxidative stress injury in human neuroblastoma SH‐SY5Y cells at low concentrations; however, C4 exhibited significant toxicity against four human tumor cells at a higher concentration in all treatments, and the range of IC50 value was 7.91 to 13.35 μM.