Weanling stress and toxicosis, which are harmful to the health of pigs’ intestines, are associated with oxidative stress. Quercetin (Que) is a polyphenolic compound that shows good anti-cancer, anti-inflammation and anti-oxidation effects. This study aimed to elaborate whether or not Que promotes IPEC-J2 (intestinal porcine enterocyte cells) proliferation and protects IPEC-J2 from oxidative damage. Thus, we examined the effects of Que on proliferation and H2O2-induced apoptosis in IPEC-J2. The results showed that Que increased IPEC-J2 viabililty, propelled cells from G1 phase into S phase and down-regulated gene levels of P27 and P21, respectively. Besides, H2O2-induced cell damage was alleviated by Que after different exposure times, and Que depressed apoptosis rate, reactive oxygen species (ROS) level and percentage of G1 phase cells and elevated the percentage of cells in G2 phase and S phase and mitochondrial membrane potential (Δψm) after IPEC-J2 exposure to H2O2. Meanwhile, Que reduced the value of Bax/Bcl-2 in H2O2 exposed cells. In low-degree oxidative damage cells, lipid peroxidation product malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were increased. In turn, Que could reverse the change of MDA content and SOD activity in low-degree damage cells. Nevertheless, catalase (CAT) activity was not changed in IPEC-J2 incubated with Que under low-degree damage conditions. Interestingly, relative expressive levels of the proteins claudin-1 and occludin were not altered under low-degree damage conditions, but Que could improve claudin-1 and occludin levels, slightly. This research indicates that Que can be greatly beneficial for intestinal porcine enterocyte cell proliferation and it protects intestinal porcine enterocyte cells from oxidation-induced apoptosis, and could be used as a potential feed additive for porcine intestinal health against pathogenic factor-induced oxidative damages and apoptosis.

Fumonisins (Fums) are mycotoxins widely distributed in crops and feed, and ingestion of Fums-contaminated crops is harmful to animal health. The purpose of this study is to explore the effect of Fum B 1 (FB 1 ) on barrier functions of porcine intestinal epithelial cells, IPEC-J2, to clarify the intestinal toxicity of Fums in pigs. The results

PTEN expression is down-regulated in HCC cell lines probably due to loss of activity of PTEN promoter.

The parts-per-billion-level nitric oxide (NO) gas sensing capability of a copper-ion-doped polyaniline/tungsten oxide nanocomposite (Cu2+/PANI/WO3) film coated on a Rayleigh surface acoustic wave device was investigated. The sensor developed in this study was sensitive to NO gas at room temperature in dry nitrogen. The surface morphology, dopant distribution, and electric properties were characterized using scanning electron microscopy, energy-dispersive X-ray spectroscopy mapping, and Hall effect measurements, respectively. The Cu2+/PANI/WO3 film exhibited high NO gas sensitivity and selectivity as well as long-term stability. At 1 ppb of NO, a signal with a frequency shift of 4.3 ppm and a signal-to-noise ratio of 17 was observed. The sensor exhibited distinct selectivity toward NO gas with no substantial response to O2, NH3 and CO2 gases.

The purpose of this study was to explore the investigative mechanism of salidroside (SAL) on LPS-induced acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). The exosomes from RLE-6TN are extracted and identified by transmission electron microscopy, particle size analysis and protein marker detection, and co-cultured with NR8383 cells. The ALI/ARDS model of SD rats was established by LPS (10 mg/kg) intratracheal instillation. Following a four-hour intratracheal instillation of LPS, 50 μl of RLE-6TN exosomes were injected through the tail vein. After that, SAL and miR-146a antagomir were injected into the tail vein for 72 h, respectively. As the changes of HE stain, body weight and ALI score are observed. The expression of miR-146a, TLR4, NF-kB, IRAK1, TRAF6 and their related proteins were detected by RT-PCR and Western blot, respectively. TNF-α, IL-6, IL-8 and IL-1 β inflammatory factors were detected by ELISA. The expression of miR-146a, NF-kB, IRAK, TRAF6 and related inflammatory factors in LPS-induced NR8383 was significantly higher than that in the control group, while SAL has greatly reduced the expression of TLR4 mediated NF-kB inflammatory pathway and related inflammatory factors. SAL can significantly improve the LPS-induced lung morphological abnormalities, slowed down the rate of weight loss in rats, and reducing the ALI score. The expression trend of NF-kB, IRAK, TRAF6 and related inflammatory factors in rats’ lung tissues was consistent with that in NR8383 cells. SAL has a protective effect on ALI/ARDS caused by sepsis, which is likely to be developed to a potential treatment for the disease. To sum up, this study provides a new theoretical basis for the treatment of ALI/ARDS with SAL.

Fumonisins (Fums) are types of mycotoxin that widely contaminante feed material crops, and can trigger potential biological toxicities to humans and various animals. However, the toxicity of Fums on porcine blood vessels has not been fully explored. Fumonisin B1 (FB1) is the main component of Fums. Therefore, the aim of this study was to explore the effects of FB1 on the oxidative stress and tight junctions of the pig iliac endothelial cells (PIECs) in vitro. The results showed that FB1 reduced the viability of PIECs, increased the contents of lipid peroxidation product malondialdehyde (MDA), decreased the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thioredoxin reductase (TrxR), and decreased the level of glutathione (GSH). In addition, the barrier functions were destroyed, along with the down-regulations on Claudin 1, Occludin and ZO-1 and the increase of paracellular permeability. Thus, this research indicates that FB1 facilitates oxidative stress and breaks barrier functions to damage pig iliac endothelium cells.

ABSTRACT. The aim of the study was to investigate the grass carp hemorrhagic infection pathway and its key-related genes. Grass carp reovirus (GCRV) might cause hemorrhagic disease in grass carps. Healthy grass carp fingerlings (N = 60) were divided into control and infected groups. Fish in the control group were intraperitoneally (ip) injected with 0.6% fish physiological saline; the infected group received 5,000,000 50% tissue culture infective doses of GCRV 873 standard strain, a double-stranded RNA (dsRNA) virus strain, ip, in 0.5 mL. Illumina HiSeq TM 2000 was used for transcriptome sequencing, and real-time polymerase chain reaction (PCR) used to detect complement factors II (C2), III (C3), and V (C5); profibrinolysin (PLG); and coagulation factor II (F2) expression. A total of 2,722,223 reads were detected in the control group, and 2,751,111 in the infected group. Among 11,023 unigenes obtained after transcriptome assembly, 10,021 unigenes were significantly differentially expressed. Gene ontology and KEGG analysis, a collection of databases dealing with genomes and biological pathways, were performed to classify unigenes into functional categories, to understand gene function and identify regulatory pathways. Real-time PCR analysis showed that C2, C3, C5, PLG, and F2 expression levels were down-regulated, confirming results of pathway-enrichment analysis. This is the first application of highthroughput sequencing technology to investigate the in vivo effects of GCRV, on genes and pathways involved in the immune response to infection in grass carp.

Sirtuin 3 (SIRT3), a mitochondrial deacetylase, is a key regulator of energy metabolism in the liver. In nonruminants, the hepatic abundance of SIRT3 is decreased in individuals with nonalcoholic fatty liver diseases, and recovery of SIRT3 alleviates hepatic triacylglycerol (TG) deposition. However, the level of SIRT3 expression and its effects on lipid metabolism in dairy cows have not been characterized. Here we studied the hepatic expression of SIRT3 in cows with fatty liver and the role of SIRT3 in fatty acid metabolism in bovine hepatocytes. This in vivo study involved 10 healthy cows and 10 cows with fatty liver, from which we collected samples of liver tissue and blood. Primary hepatocytes were isolated from Holstein calves and treated with 0, 0.5, or 1.0 mM nonesterified fatty acids (NEFA) for 24 h or transinfected with SIRT3 overexpression adenovirus (Ad-SIRT3)/SIRT3-short interfering (si)RNA for 48 h. Cows with fatty liver displayed lower serum glucose concentrations but higher serum NEFA and β-hydroxybutyrate concentrations relative to healthy cows. Cows with fatty liver also had significant lower mRNA and protein abundance of hepatic SIRT3. Incubation of primary hepatocytes with NEFA reduced SIRT3 abundance in primary hepatocytes in a dose-dependent manner. Fatty acid (1 mM) treatment also markedly increased the abundance of acetyl-CoA carboxylase 1 (ACC1) and fatty acid synthase (FAS) but significantly decreased the abundance of carnitine palmitoyltransferase I (CPT1A), carnitine palmitoyltransferase II (CPT2), and acyl-CoA oxidase (ACO). Knockdown of SIRT3 by SIRT3-siRNA downregulated the mRNA abundance of CPT1A, CPT2, and ACO. In contrast, overexpression of SIRT3 by Ad-SIRT3 upregulated the mRNA abundance of CPT1A, CPT2, and ACO; downregulated the mRNA abundance of ACC1 and FAS; and consequently, decreased intracellular TG concentrations. Overexpression of SIRT3 ameliorated exogenous NEFA-induced TG accumulation by downregulating the abundance of ACC1 and FAS and upregulating the abundance of CPT1A, CPT2, and ACO in calf hepatocytes. Our data demonstrated that cows with fatty liver had lower hepatic SIRT3 contents, and an increase in SIRT3 abundance by overexpression mitigated TG deposition by modulating the expression of lipid metabolism genes in bovine hepatocytes. These data suggest a possible role of SIRT3 as a therapeutic target for fatty liver disease prevention in periparturient dairy cattle.