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Excess Cu and Zn can cause many adverse effects in fish. However, few studies have addressed the effects of dietary Cu and Zn on antioxidant physiology and immunity and the underlying mechanisms in fishes. In this study, accumulation of Cu and Zn, effects on the antioxidant enzymes and the transcriptional expressions of immune-related genes were examined in the Oreochromis niloticus fed the Cu and/or Zn enriched duckweed. The results showed that the liver and intestine had the highest accumulation of Cu2+ and Zn2+ while the muscle had the lowest accumulation of these two metals. The activities of SOD, CAT, GPx and the contents of GSH, GSSG in the liver of all treatment groups were significantly decreased compared to the control group. MDA content was significantly elevated in all treatment groups after feeding for 21 days, implying lipid peroxidation in the liver. In the Cu + Zn group, the activities of SOD, GPx and the GSSG content in the liver were significantly decreased. Compared with the Zn group, the LZM activity in the Cu + Zn group was reversed after feeding for 42 days (P

BackgroundWhile tilapia are the second most farmed group of fish in the world, the Oreochromis niloticus (♀) × Oreochromis aureus (♂) hybrid is one of the most frequently observed tilapia crosses in China. Based on its conservative nature and maternal inheritance pattern, mitochondrial DNA is often used in kinship analysis. Evidence of paternal inheritance has been noted in some animal species. ResultsThe mitochondrial CoI and Cytb genes, and D-loop gene regions of Oreochromis niloticus and Oreochromis aureus fish were sequenced and aligned to their orthogonal and backcrossed offspring. As evidence of paternal mitochondria DNA inheritance was found, the whole mitochondrial genome was then sequenced. Results showed that in the Oreochromis niloticus (♀) × Oreochromis aureus (♂) hybrids, certain fish shared 92.88% of the maternal mitochondria genome, and 99.86% with the paternal mitochondria genome. This implied that there was paternal mtDNA inheritance. However, all Oreochromis niloticus (♂) × Oreochromis aureus (♀) hybrids had 100% identical mitochondria genome with their female parent. ConclusionsThe study showed that while paternal mtDNA inheritance occurred in the Oreochromis niloticus (♀) × Oreochromis aureus (♂) hybrid, this did not happen in Oreochromis niloticus (♂) × Oreochromis aureus (♀) offspring. This implies that in hybrid species, different hybridization combinations might provide an explanation for paternal mtDNA inheritance pattern.

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Insulin resistance (IR) is important in the development and progression of NAFLD. Nuclear erythroid 2‑related factor 2 (Nrf2) has previously been reported to be a novel regulator in NAFLD. The present study determined that Nrf2 knockdown accelerated the onset of obesity and non‑alcoholic steatohepatitis (NASH), via the induction of hepatic IR in mice fed a high‑fat diet (HFD), which was confirmed by an increase in total and hepatic weight in Nrf2‑null‑HFD mice, in addition to marked structural disorder in liver tissues from the Nrf2‑null‑HFD group analyzed by histopathological examination. Subsequently, it was demonstrated that hepatic IR in Nrf2‑null‑HFD mice was influenced by oxidative stress; this was confirmed by an increase in malondialdehyde levels and a decrease in glutathione levels. In addition, it was determined that the induction of hepatic IR by Nrf2 knockdown in HFD-treated mice was regulated by activation of the nuclear factor‑κB (NF‑κB) signaling pathway, as detected by an increase in the expression levels of nuclear NF‑κB, and its downstream effectors interleukin‑6 and tumor necrosis factor‑α. The present study provides insight into the function of Nrf2 in NAFLD, indicating that Nrf2 deletion may lead to hepatic IR by activation of NF‑κB, which is often associated with oxidative stress. Therefore, activation of Nrf2 may limit disease progression and act as a therapeutic approach for the treatment of NASH.

The present study aimed to investigate the protective role of curcumin against oxidative stress in rat hepatic stellate cells (HSCs)-T6, and to determine the possible underlying mechanisms. HSC-T6 cells were divided into three groups: Negative control group, oxidant-treated group and curcumin-treated group. Flow cytometry and spectrophotometry were used to measure the production of reactive oxygen species (ROS), and the levels of malondialdehyde (MDA) and glutathione (GSH). Immunocytochemistry and a radioimmunoassay were used to determine the expression of smooth muscle α-actin (α-SMA) and the secretion of extracellular matrix (ECM) molecules. In addition, western blotting and immunocytochemistry were used to determine the expression levels of nuclear factor-erythroid 2-related factor (Nrf2). Treatment with glucose oxidase (GO) significantly stimulated the formation of ROS and increased the production of MDA, as compared with the control cells; however, the production of GSH was only slightly increased. In addition, treatment with GO significantly promoted the expression of α-SMA and the secretion of ECM molecules. Conversely, treatment with curcumin significantly decreased the levels of ROS and MDA, and significantly increased the levels of GSH. Curcumin significantly inhibited the expression of α-SMA and decreased the secretion of ECM molecules. Furthermore, treatment with curcumin significantly increased the nuclear expression levels of Nrf2. These results indicated that curcumin may protect rat HSCs against oxidative stress and inhibit the GO-induced activation and secretion of ECM molecules in vitro. These effects were mediated by the upregulation of Nrf2 nuclear translocation.

Chitosan (CS) based nanoparticles (NPs) have several advantages in delivering drugs. They are usually prepared in a micro-emulsion solvent system but this route can leave significant levels of potentially harmful organic solvent residue in the NPs. In this study, we prepared CS based nanocomposites using charge driven self-assembly in an aqueous buffer, thus avoiding the use of organic solvents. Doxorubicin (DOX) was covalently attached to positive charged CS with a legumain substrate peptide to confer targeted drug release property, since legumain is often overexpressed in tumors or tumor associated micro environments. This DOX prodrug solution interacted with negative charged methoxyl poly (ethylene glycol)-block-poly (glutamic acid) copolymer (PEG-PGA) in an aqueous buffer forming nanocomposite with a regular morphology. The particle size and zeta potential of these NPs was regulated by the addition of different PEG-PGA concentrations into the DOX prodrug solution. Due to its potential for legumain triggered release, this DOX NP exhibited enhanced cytotoxicity against choroidal melanoma cell line (Mum-2C) and reduced cytotoxicity on normal human corneal epithelial cells (HCEC), suggesting a good potential for enhanced targeted delivery of chemotherapeutic agents. A chitosan based nanocomposite with legumain sensitive properties are rapidly controllable prepared in aqueous buffer by charge driven self-assembly strategy, without using micro-emulsion solvent system and cross-linking agents.

Background The SIP syncytium in the gut consists of smooth muscle cells, interstitial cells of Cajal, and PDGFRα+ cells. We studied the fate of SIP cells after blocking PDGFRα receptor to explore the roles of PDGFRα signaling in the postnatal development and functional maintenance of the SIP syncytium. Methods Crenolanib was administered to mice from P0, P10, or P50. The morphological changes in SIP cells were examined by immunofluorescence. Protein expression in SIP cells was detected by Western blotting. Moreover, colonic transit was analyzed by testing the colonic bead expulsion time. Key results A dose of 5 mg(kg•day)-1 crenolanib administered for 10 days beginning on P0 apparently hindered the development of PDGFRα+ cells in the colonic longitudinal muscularis and myenteric plexus without influencing their proliferative activity and apoptosis, but this result was not seen in the colonic circular muscularis. SMCs were also inhibited by crenolanib. A dose of 7.5 mg(kg•day)-1 crenolanib administered for 15 days beginning on P0 caused reductions in both PDGFRα+ cells and ICC in the longitudinal muscularis, myenteric plexus, and circular muscularis. However, when crenolanib was administered at a dose of 5 mg(kg•day)-1 beginning on P10 or P50, it only noticeably decreased the number of PDGFRα+ cells in the colonic longitudinal muscularis. Crenolanib also caused PDGFRα+ cells to transdifferentiate into SMC in adult mice. Colonic transit was delayed after administration of crenolanib. Conclusions & inferences Therefore, PDGFRα signaling is essential for the development and functional maintenance of the SIP cells, especially PDGFRα+ cells.

In this paper,the high performance liquid chromatography(HPLC) was used to monitor the spatial and temporal distribution of dissolved Microcystin-LR and Microcystin-RR in Lake Taihu,and its relationship with physiochemical factors of the lake were also discussed.The results showed that the concentrations of microcystin(MCs) were not different between surface and bottom water in a day,and the highest concentration of microcystins occurred in winter.Concentrations of the MCs changed much during one year in the sampling sites N5 and N1 which located in Zhushan Bay and the western part of Lake Taihu,respectively.Generally,the concentration of the MC-LR was higher than MC-RR for the year in average while the opposite results appeared in individual month of August and September.Correlation analysis showed that MC-LR was significantly positive correlated with TN,but did not show correlation with TP.During the period of water bloom of cyanobacteria,levels of the MC-LR were significantly positive correlated with TP,TN,UV254,SS,total organic carbon and biomass of cyanobacteria,whereas MC-RR was not significant correlated with all the environmental factors in the statistical test.

A sulfated polysaccharide (EI-SP), extracted from Enteromorpha intestinalis that is a kind of algae, is found to have anticancer activity. This study was designed to investigate the anti-tumor effect of EI-SP on human hepatoma HepG2 cell line and its possible mechanisms. An MTT assay showed that EI-SP could specifically inhibit the growth of human hepatoma HepG2 cells in a dose-dependent manner. Analysis by flow cytometry indicated that the apoptosis of tumor cells increased after treatment with EI-SP in range of 100–400 μg/ml. Furthermore, Western blot analysis showed that EI-SP treatment led to decreased protein expression of Bcl-2 and an increase in Bax, cleaved caspase-3, cleaved caspase-9 and cleaved poly(ADP-ribose) polymerase (PARP). Moreover, it was found that EI-SP caused a loss of mitochondrial membrane potential (Δψ m) and the release of cytochrome c to the cytosol. Collectively, our results showed that the EI-SP induces apoptosis in HepG2 cells involving a caspases-mediated mitochondrial signalling pathway.