摘要：
Our previous studies have found that fish oil rich in omega-3 polyunsaturated fatty acids (omega-3 PUFA) protects against non-alcoholic fatty liver disease (NAFLD) in mice. This study was aimed to explore the effects of fish oil on high fat diet (HFD)-induced circadian bile composition chaos. Male C57BL/6 mice were randomly divided into three groups, a control group (CON), a HFD group and a fish oil (FO) group, which were fed a normal chow diet, a HFD, and a HFD supplemented with FO, respectively for 12 weeks. At the end of the experiment, liver tissue, blood and bile samples were processed at 12-h intervals with the first one at zeitgeber time 0 (ZT0) and the second at zeitgeber time 12 (ZT12). Metabolites in bile were determined using UPLC-QTOF-MS, screened using multivariate statistical analysis, and analyzed using KEGG database and Metaboanalyst. The expression levels of key proteins in bile acid metabolism were examined using western blot. Results of biochemical analysis and H&E staining illustrated that feeding of HFD induced NAFLD, which was ameliorated in FO group. The bile content of each group at ZT0 (CON, HFD, or FO group) was respectively higher than that at ZT12 (P<.05). The metabolic pathway analysis of differential metabolites showed that these differences were correlated with amino acid metabolism, fatty acid biosynthesis and primary bile acid synthesis at ZT0. FO supplement could modify bile composition, which was related to the influence of its omega-3 PUFA on liver metabolism. omega-3 PUFA may also regulate the circadian rhythm of bile metabolism.
摘要：
Listeria monocytogenes (L. monocytogenes) is a well-known food-borne pathogen that causes systemic listeriosis. Its biofilm-forming ability is known to be important for its antimicrobial resistance and persistence. Epigallocatechin-gallate (EGCG) is the highest component of tea polyphenols in tea extracts and has broad-spectrum antimicrobial activities. In this study, the efficacys of EGCG to inhibit biofilm formation and hemolytic activity of L. monocytogenes were determined. EGCG at 20 mu g/mL, 40 mu g/mL (less than compound's minimum inhibitory concentration, MIC) and 200 mu g/mL (1 MIC) were tested. Crystal violet staining showed that sub-MIC and MIC of EGCG could significantly reduce the biofilm formation by L. monocytogenes on polystyrene microtiter plates at three temperatures (15 degrees C, 30 degrees C and 37 degrees C). EGCG reduced the sessile cell numbers present in biofilm at those temperatures. EGCG also significantly inhibited hemolytic activity of L. monocytogenes as measured by sheep red blood cells. Real time PCR assay was used to investigate the relative gene expression of L monocytogenes grown at 37 degrees C and revealed that EGCG down-regulated virulence genes (inlA and hly), SOS response genes (recA and yneA) and quorum sensing gene (agrA). These results suggested the feasibility of using EGCG in food industry to control L monocytogenes biofilm formation. (C) 2017 Elsevier Ltd. All rights reserved.
摘要：
Paenibacterin is a novel antimicrobial lipopeptide produced by Paenibacillus thiaminolyticus. The present study assesses the efficacy of paenibacterin in inhibiting Listeria monocytogenes biofilm formation and removing established biofilm. Paenibacterin at 1.7 mu g/mL (less than compound's minimum inhibitory concentration, MIC) and higher concentrations (3.4 mu g/mL, 6.8 mu g/mL) were tested. Concentrations greater than the lipopeptide's MIC significantly inhibited the formation of L. monocytogenes biofilm on polystyrene microtiter plates at 30 degrees C and 37 degrees C. Paenibacterin also was added to established biofilm and its structure or removal was monitored by fluorescence microscopes after appropriate staining. Results show that paenibacterin could eliminate established biofilms formed at 30 degrees C for 72 h, whereas it could not disrupt stronger biofilms formed at 37. degrees C for 72 h. Motility of L. monocytogenes is important for its ability to form biofilm. Swimming assay confirmed that paenibacterin suppressed L. monocytogenes motility. Real time quantitative PCR data revealed that paenibacterin down-regulated L. monocytogenes critical biofilm-associated genes, prfA, agrA, flail, fliG and flgE. These results suggested the feasibility of using paenibacterin in food processing environments to control L. monocytogenes growth and biofilm formation, or even for removal of some established biofilms. (C) 2017 Elsevier Ltd. All rights reserved.
摘要：
Objective: To explore the toxicity of multi-walled carbon nanotubes (MWCNTs) on the liver lipid metabolism of offspring mice and the possible mechanisms involved. Method: Virgin female (16–18 g) and male (18–20 g) C57BL/6 mice were randomly divided into two groups: Control group and Test group. After anesthesia with chloral hydrate, the mice were administered 50 μL saline or dust solution by intratracheal instillation (Control group: 50 μL saline; Test group: 15 mg kg−1 MWCNTs). Mice were injected with these doses once a week for 13 weeks. Then, male and female mice in the same group were allowed to mate to produce offspring. The pups were fed with normal diet until the end of the experiment (12 weeks old). The offspring mice were sacrificed by decapitation to detect the blood biochemistry and the expression of genes and proteins. Results: Compared with the Control group, MWCNTs significantly reduced the weight of offspring mice (male and female) and led to histopathological changes in the liver tissues. The expression of liver fat synthesis gene significantly increased (P < 0.05 or P < 0.01). The expression of genes and proteins involved in the inflammatory reactions appeared to be abnormal (P < 0.05 or P < 0.01). Conclusion: Exposure of adult mice to MWCNTs can affect the expression of fatty acid synthesis genes in the liver tissues of offspring mice, leading to disruption of liver function and accumulation of lipid droplets in the hepatocytes. The imbalance between M1 and M2 liver macrophage phenotypes may be one of the underlying mechanisms of action of MWCNTs leading to disordered fatty acid synthesis in offspring mice.
Objective: To explore the toxicity of multi-walled carbon nanotubes (MWCNTs) on the liver lipid metabolism of offspring mice and the possible mechanisms involved.
作者机构：
[Wang, Hualin; Liu, Zhiguo] Wuhan Polytech Univ, Sch Biol & Pharmaceut Engn, Wuhan, Hubei, Peoples R China.;[Wang, Hualin; Wan, Jennifer Man-Fan; Sit, Wat-Hung] Univ Hong Kong, Sch Biol Sci, Food & Nutr Div, Hong Kong, Hong Kong, Peoples R China.;[Tipoe, George Lim] Univ Hong Kong, Li Ka Shing Fac Med, Dept Anat, Hong Kong, Hong Kong, Peoples R China.
通讯机构：
[Wan, Jennifer Man-Fan] U;Univ Hong Kong, Sch Biol Sci, Food & Nutr Div, Hong Kong, Hong Kong, Peoples R China.
摘要：
Introduction: The influences of dietary fatty acids on the progress of chronic liver diseases have attracted lots of attentions, but the mechanisms of the effects of lipids rich in saturated fatty acids or PUFAs on hepatic fibrogenesis remain unclear. Methods: Female Fischer 344 rats were fed normal chow or chow plus 20% (w/w) of corn oil or lard, respectively, and injected CCl4 twice a week for 4 weeks to induce liver fibrosis. Masson's staining was adopted to illustrate the fibrosis level. The mRNA expression level of alpha-SMA and the DNA methylation level of its promoter region were analyzed. A 2-DE gel based proteomic approach was constructed to investigate the differential expression level of hepatic proteome between three diet groups. Results: Histological evaluations and alpha-SMA expression analysis illustrated the high corn oil intake has no effects on hepatic fibrogenesis, but lard intake aggravated liver fibrosis, partly attributed to DNA demethylation of alpha-SMA promoter region. 2-DE Gel based proteomic study demonstrated excessive lard consumption elevated the expression of fibrosis related alpha-1-antitrypsin precursor, and endoplasmic reticulum stress related proteins such as heat shock cognate 71 kDa, eukaryotic translation initiation factor 4A1 and protein disulfide isomerase associated 3. Moreover, unlike corn oil rich in PUFAs, lard had no effects to elevate the expression of glutathione S-transferases, but decreased the expression of iron store related proteins heme binding protein 1 and ferritin. Conclusions: Lard intake aggravates CCl4 induced liver fibrosis via enhancing the expression of fibrogenesis and ER stress related proteins, and disturbing the hepatic transmethylation reaction. (C) 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
摘要：
<jats:p>Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases worldwide. Recent studies have indicated that fish oil supplementation has benefits against NAFLD. Our previous transcriptomic study has validated the effect of fish oil supplementation on altering hepatic gene expression in a NAFLD rat model. In the current study, we examined the effects of fish oil on the expression of hepatic microRNAs. Male Sprague–Dawley rats were fed with a lab chow (CON), high-fat high-cholesterol diet (WD), or WD supplemented with fish oil (FOH), respectively. Small RNAs were extracted from livers for RNA-sequencing. A total of 79 miRNAs were identified as differentially expressed miRNAs (DEMs) between FOH and WD groups, exemplified by rno-miR-29c-3p, rno-miR-30d-5p, rno-miR-33-5p, rno-miR-34a, and rno-miR-328a-3p. Functional annotation of DEMs predicted target genes suggested that the altered hepatic miRNAs contributed to fish oil modification of hepatic lipid metabolism and signaling transduction. Integrative analysis of DEMs and differentially expressed genes suggested that the expression difference of<jats:italic> Pcsk9, Insig2, Per3,</jats:italic> and<jats:italic> Socs1/3</jats:italic> between FOH and WD groups may be due to miRNA modification. Our study reveals that fish oil supplementation alters hepatic expression of miRNAs, which may contribute to fish oil amelioration of NAFLD in rats.</jats:p>
摘要：
Cytotoxic effects of ZnO nanoparticles on mouse testicular cells Zhe Han,1,* Qi Yan,1,* Wei Ge,2 Zhi-Guo Liu,1 Sangiliyandi Gurunathan,3 Massimo De Felici,4 Wei Shen,2 Xi-Feng Zhang1 1College of Biological and Pharmaceutical Engineering, Wuhan Polytechnic University, Wuhan, People’s Republic of China; 2Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, College of Animal Science and Technology, Qingdao Agricultural University, Qingdao, People’s Republic of China; 3Department of Stem Cell and Regenerative Biology, Konkuk University, Seoul, Republic of Korea; 4Department of Biomedicine and Prevention, University of Rome “Tor Vergata”, Rome, Italy *These authors contributed equally tothis work Background: Nanoscience and nanotechnology are developing rapidly, and the applications of nanoparticles (NPs) have been found in several fields. At present, NPs are widely used in traditional consumer and industrial products, however, the properties and safety of NPs are still unclear and there are concerns about their potential environmental and health effects. The aim of the present study was to investigate the potential toxicity of ZnO NPs on testicular cells using both in vitro and in vivo systems in a mouse experimental model. Methods: ZnO NPs with a crystalline size of 70 nm were characterized with various analytical techniques, including ultraviolet-visible spectroscopy, Fourier transform infrared spectroscopy, X-ray diffraction, transmission electron microscopy, and atomic force microscopy. The cytotoxicity of the ZnO NPs was examined in vitro on Leydig cell and Sertoli cell lines, and in vivo on the testes of CD1 mice injected with single doses of ZnO NPs.Results: ZnO NPs were internalized by Leydig cells and Sertoli cells, and this resulted in cytotoxicity in a time- and dose-dependent manner through the induction of apoptosis. Apoptosis likely occurred as a consequence of DNA damage (detected as γ-H2AX and RAD51 foci) caused by increase in reactive oxygen species associated with loss of mitochondrial membrane potential. In addition, injection of ZnO NPs in male mice caused structural alterations in the seminiferous epithelium and sperm abnormalities.Conclusion: These results demonstrate that ZnO NPs have the potential to induce apoptosis in testicular cells likely through DNA damage caused by reactive oxygen species, with possible adverse consequences for spermatogenesis and therefore, male fertility. This suggests that evaluating the potential impacts of engineered NPs is essential prior to their mass production, to address both the environmental and human health concerns and also to develop sustainable and safer nanomaterials. Keywords: ZnO nanoparticle, Sertoli cells, Leydig cells, mice
