ObjectiveTo investigate the effects of scavenger receptor A on the catabolism of lipid emulsions and further to see if it differently affects long-chain triglyceride (LCT) and fish oil (FO) emulsions. MethodsA total of 24 C57BL/6J female mice, 10 to 12 weeks old, were randomly divided into 4 groups with 6 mice in each group. Two groups of mice were intravenously injected with dextran sulfate ( DexSO4 ) ( 1 mg/mouse) followed by intravenous injection of [1α, 2α(n)-3H] cholesteryl oleoyl ether [(3H)CEt] labelled LCT or FO emulsions (0.4mg triglycerde/mouse) at 2 minutes respectively, and other two groups were injected by saline as controls before injection of (3H)CEt labelled LCT and FO emulsions. Then, blood was drawn at fixed intervals to measure the radioactivities and the emulsion's fractional catabolic rates (FCR) were calculated. With the same procedures above mentioned, non-radiolabelled LCT and FO emulsions were intravenously injected to mice to determine liver uptake of lipid emulsions under electromicroscopy. Finally, THP1 cell line was used to examine the effects of DexSO4 on cell uptake of LCT and FO emulsions in vitro. ResultsPre-injection of DexSO4 to mice decreased the FCR of both LCT and FO emulsions at 72.38％ and 47.38％ respectively, as compared to controls ( P =0.020 ). Electromicroscopy showed that pre-injection of DexS04 decreased the uptakes of LCT and FO emulsions by Kupffer cells and sinusoidal endothelial cells similarly. In hepatocytes, no lipid droplets existed in mice with LCT emulsion injection, whereas some lipid droplets were still shown in mice with FO emulsions but with less quantities compared to control mice.In vitro, addition of DexSO4 to medium decreased THP1 cell uptakes of LCT and FO emulsions ( P =0.003 and 0.008) by 30.74％ and 41.60％ respectively. However, no differences were found in the effects of DexS04 on cell uptakes between LCT and FO emulsions ( P =0.080). ConclusionScavenger receptor A plays important roles in catabolism of lipid emulsions to some extent, and it's effects on FO emulsions may be less than LCT emulsions.

Objective:To investigate the effect of miRNA-106b (miR-106b) on human laryngeal squamous cell carcinoma Hep-2 and TU212 cells and its mechanism.Methods:Hep-2 and TU212 cells were divided into miR-106b inhibitory sequence transfected group (the experimental group), miR-106b competitive negative sequence transfected group (the negative control group) and non-intervention group (the blank group). The inhibitory effect of miR-106b inhibitory sequence on the expression of miR-106b was verified by using reverse transcription quantitative polymerase chain reaction (qRT-PCR). Whether phosphatase and tensin homolog (PTEN) was the target gene of miR-106b was analyzed by using bioinformatics and luciferase report vector. PTEN small interfering RNA (siRNA) was used to inhibit the expression of PTEN in Hep-2 and TU212 cells. Transwell method and Western blot were used to detect the change of invasion ability of Hep-2 and TU212 cells after miR-106b silencing or the PTEN intervening, and the expression change of PTEN, epithelial cadherin and vimentin.Results:The relative expression levels of miR-106b in Hep-2 and TU212 cells in the experimental group were 0.110 ± 0.037 and 0.074 ± 0.009, respectively, which were lower than those in the negative control group (1.013±0.059 and 1.035±0.062, respectively; all P < 0.05). In Transwell experiments, the number of invasive cells in each field of Hep-2 and TU212 cells in the experimental group was less than that in the negative control group [(37.09±4.02) vs. (95.65±4.77), (29.16±2.49) vs. (103.19±6.08), all P < 0.05]. The bioinformatics analysis results showed that 3'-UTR region of PTEN mRNA was complementary to 3'-UTR region of miR-106b. Dual-luciferase reporter system analysis showed that the luciferase reporter activity of wild-type PTEN gene transfected with miR-106b was decreased to (22.84±2.68)%, and that of mutant PTEN gene transfected with miR-106b was almost unchanged [(92.08±3.44)%], and the difference was statistically significant ( P < 0.001). The expression level of PTEN protein of Hep-2 and TU212 cells in the experimental group was higher than that in the negative control group. Transwell method showed that the number of invasive cells in each field of Hep-2 and TU212 cells in the experimental group with the inhibition of PTEN expression was more than that in the experimental group without the inhibition of PTEN expression [(65.08±3.57) vs. (26.72±2.58), (57.38±4.96) vs. (31.81±2.97), all P < 0.05]. Western blot showed that the expression level of epithelial-cadherin was up-regulated and vimentin was down-regulated of Hep-2 and TU212 cells in the experimental group with the inhibition of PTEN expression. Conclusions:The human laryngeal squamous cell carcinoma Hep-2 and TU212 cell miR-106b can influence the downstream invasion-related protein of PTEN and change the cell invasion ability through the targeted regulation of PTEN expression.