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Autophagy is a conserved proteolytic mechanism, which degrades and recycles damaged organs and proteins in cells to resist external stress. Probiotics could induce autophagy; however, its underlying molecular mechanisms remain elusive. Our previous study has found that BaSC06 could alleviate oxidative stress by inducing autophagy in rats. This research aimed to verify whether Bacillus amyloliquefaciens SC06 can induce autophagy to alleviate oxidative stress in IPEC-J2 cells, as well as explore its mechanisms. IPEC-J2 cells were first pretreated with 108 CFU/mL BaSC06, and then were induced to oxidative stress by the optimal dose of diquat. The results showed that BaSC06 significantly triggered autophagy, indicated by the up-regulation of LC3 and Beclin1 along with downregulation of p62 in IPEC-J2 cells. Further analysis revealed that BaSC06 inhibited the AKT–FOXO signaling pathway by inhibiting the expression of p-AKT and p-FOXO and inducing the expression of SIRT1, resulting in increasing the transcriptional activity of FOXO3 and gene expression of the ATG5–ATG12 complex to induce autophagy, which alleviated oxidative stress and apoptosis. Taken together, BaSC06 can induce AKT–FOXO-mediated autophagy to alleviate oxidative stress-induced apoptosis and cell damage, thus providing novel theoretical support for probiotics in the prevention and treatment of oxidative damage.

Background: This study on interprofessional relationships took place in Eastern Kentucky analyzing optometry, medical and nursing students at the University of Pikeville.  The Readiness for Interprofessional Learning Scale (RIPLS), regarding all three healthcare professional schools, was used to measure and determine students' views on working with one another.  The purpose of the study was to examine similarities and differences in student attitudes across the three health professional programs within the same university. Methods: Second year University of Pikeville (UPIKE) nursing, optometry, and medical students were given survey questions that followed the validated 19-item Readiness for Interprofessional Learning Scale (RIPLS). Results: While the optometry and medical students demonstrated statistically similar attitudes, key statistical findings included that nursing students were more likely than medical students to believe that clinical problem solving can only be learned effectively with students/professionals from their own school/organization (p = 0.015);  nursing students were more likely than medical students to welcome the opportunity to work on small group projects with other health and social care students/professionals (p = 0.018); and nursing students were more likely than both optometry and medical students to not be sure what their professional role will be/is  (p=.005). Conclusions: At the UPIKE, there is an observable difference between the attitudes toward IPE. Nursing students appeared to have a more positive attitude toward IPE than medical and optometry students, with the medical and optometry students having similar attitudes.

Heat shock proteins (HSPs) are a set of highly conserved proteins that can serve as intestinal gate keepers in gut homeostasis. Here, effects of a probiotic, Lactobacillus rhamnosus GG (LGG), and two novel porcine isolates, Lactobacillus johnsonii strain P47‐HY and Lactobacillus reuteri strain P43‐HUV, on cytoprotective HSP expression and gut barrier function, were investigated in a porcine IPEC‐J2 intestinal epithelial cell line model. The IPEC‐J2 cells polarized on a permeable filter exhibited villus‐like cell phenotype with development of apical microvilli. Western blot analysis detected HSP expression in IPEC‐J2 and revealed that L. johnsonii and L. reuteri strains were able to significantly induce HSP27, despite high basal expression in IPEC‐J2, whereas LGG did not. For HSP72, only the supernatant of L. reuteri induced the expression, which was comparable to the heat shock treatment, which indicated that HSP72 expression was more stimulus specific. The protective effect of lactobacilli was further studied in IPEC‐J2 under an enterotoxigenic Escherichia coli (ETEC) challenge. ETEC caused intestinal barrier destruction, as reflected by loss of cell–cell contact, reduced IPEC‐J2 cell viability and transepithelial electrical resistance, and disruption of tight junction protein zonula occludens‐1. In contrast, the L. reuteri treatment substantially counteracted these detrimental effects and preserved the barrier function. L. johnsonii and LGG also achieved barrier protection, partly by directly inhibiting ETEC attachment. Together, the results indicate that specific strains of Lactobacillus can enhance gut barrier function through cytoprotective HSP induction and fortify the cell protection against ETEC challenge through tight junction protein modulation and direct interaction with pathogens. Lactobacilli induce heat shock protein HSP27 and protect IPEC‐J2 cells from disruption of tight junction protein under an enterotoxigenic Escherichia coli challenge.

Zearalenone (ZEN) is a widespread contaminant of cereals and agricultural products which causes food safety issues. Ingesting food or feed contaminated with ZEN can disrupt the intestinal epithelial barrier function. The RhoA/ROCK signaling pathway plays a key role in regulating the epithelial barrier function, but studies on such roles have rarely focused on the intestine. The aim of this experiment was to investigate the exact mechanism of ZEN-induced intestinal barrier damage and whether the RhoA/ROCK signaling pathway is involved. The results showed that ZEN significantly induced alkaline phosphatase (AP) activity and FITC–dextran (4 kDa) passage across the epithelial barrier, which significantly reduced the transepithelial resistance (TEER). Meanwhile, ZEN could induce the significantly down-regulated mRNA expression of tight junction proteins (occludin, claudin-1, ZO-1, and claudin-3) and redistribution of ZO-1 immunofluorescence. Further studies demonstrated that ZEN exposure activated the RhoA/ROCK signaling pathway, significantly up-regulated the mRNA expression of ROCK1, the main effector of the signaling pathway, the protein expression of phosphorylated myosin light chain (MLC) and myosin light chain kinase (MLCK), and relatively increased the activity of ATP in cells, simultaneously remodeling the cytoskeleton (F-actin). Overall, our study indicated that ZEN induced intestinal barrier dysfunction by activating the RhoA/ROCK signaling pathway.

Oxidative stress can adversely affect the health status of the body, more specifically by causing intestinal damage by disrupting the permeability of the intestinal barrier. This is closely related to intestinal epithelial cell apoptosis caused by the mass production of reactive oxygen species (ROS). Baicalin (Bai) is a major active ingredient in Chinese traditional herbal medicine that has antioxidant, anti-inflammatory, and anti-cancer properties. The purpose of this study was to explore the underlying mechanisms by which Bai protects against hydrogen peroxide (H2O2)-induced intestinal injury in vitro. Our results indicated that H2O2 treatment caused injury to IPEC-J2 cells, resulting in their apoptosis. However, Bai treatment attenuated H2O2-induced IPEC-J2 cell damage by up-regulating the mRNA and protein expression of ZO-1, Occludin, and Claudin1. Besides, Bai treatment prevented H2O2-induced ROS and MDA production and increased the activities of antioxidant enzymes (SOD, CAT, and GSH-PX). Moreover, Bai treatment also attenuated H2O2-induced apoptosis in IPEC-J2 cells by down-regulating the mRNA expression of Caspase-3 and Caspase-9 and up-regulating the mRNA expression of FAS and Bax, which are involved in the inhibition of mitochondrial pathways. The expression of Nrf2 increased after treatment with H2O2, and Bai can alleviate this phenomenon. Meanwhile, Bai down-regulated the ratio of phosphorylated AMPK to unphosphorylated AMPK, which is indicative of the mRNA abundance of antioxidant-related genes. In addition, knockdown of AMPK by short-hairpin RNA (shRNA) significantly reduced the protein levels of AMPK and Nrf2, increased the percentage of apoptotic cells, and abrogated Bai-mediated protection against oxidative stress. Collectively, our results indicated that Bai attenuated H2O2-induced cell injury and apoptosis in IPEC-J2 cells through improving the antioxidant capacity through the inhibition of the oxidative stress-mediated AMPK/Nrf2 signaling pathway.

Background Tight junctions (TJs) maintain the intestinal mucosal barrier, dysfunction of which plays a vital role in the pathophysiology of a variety of gastrointestinal disorders. Previously, we have shown that L. reuteri I5007 maintained the gut epithelial barrier in newborn piglets. Here we aimed to decipher the influence of L. reuteri I5007 on tight junction (TJ) protein expression both in vivo and in vitro . Results We found that L. reuteri I5007 significantly increased the protein abundance of intestinal epithelial claudin-1, occludin and zonula occluden-1 (ZO-1) in newborn piglets (orally administrated with 6 × 10 9  CFU of L. reuteri I5007 daily for 14 days). In vitro , treatment with L. reuteri I5007 alone maintained the transepithelial electrical resistance (TEER) of IPEC-J2 cells with time. In addition, IPEC-J2 cells were stimulated with 1 μg/mL lipopolysaccharide (LPS) for 1, 4, 8, 12 or 24 h, following pre-treatment with L. reuteri I5007 or its culture supernatant for 2 h. The results showed that LPS time-dependently induced (significantly after 4 or 8 h) the expression of TNF-α and IL-6, and decreased TJ proteins, which was reversed by pre-treatment of L. reuteri I5007 or its culture supernatant. Conclusions L. reuteri I5007 had beneficial effects on the expression of TJ proteins in newborn piglets and the in-vitro results showed this strain had a positive effect on TEER of cells and inhibited the reduction of TJ proteins expression induced by LPS. These findings indicated L. reuteri I5007 may have potential roles in protection TJ proteins in TJ-deficient conditions.

The present study compared the protective effect of sodium selenite (SS) and selenomethionine (SeMet) on heat stress (HS)-invoked porcine IPEC-J2 cellular damage and integrate potential roles of corresponding selenoprotein. Cells were cultured at 37°C until 80 % confluence and then subjected to four different conditions for 24 h: at 37°C (control), 41·5°C (HS), 41·5°C supplied with 0·42 µmol Se/L SS (SS), or SeMet (SeMet). HS significantly decreased cell viability, up-regulated mRNA and protein levels of heat shock protein 70 (HSP70) and down-regulated mRNA and protein levels of tight junction-related proteins (claudin-1 (CLDN-1) and zonula occludens-1 (ZO-1)). HS-induced cell injury was associated with the up-regulation ( P < 0·05) of six inflammation-related genes and fourteen selenoprotein encoding genes and down-regulation ( P < 0·05) of two inflammation-related genes and five selenoprotein encoding genes. Compared with the HS group, SS and SeMet supplementation resulted in an increase ( P < 0·05) in cell viability, decreased ( P < 0·05) mRNA expression of HSP70 and six inflammation-related genes and rescue ( P < 0·05) of mRNA and protein levels of CLDN-1 and ZO-1. SS and SeMet supplementation changes the expressions of nineteen selenoprotein encoding genes in cells affected by HS. Both Se supplementation significantly recovered the protein level of glutathione peroxidase-1 and increased selenoprotein P in the IPEC-J2 cells under HS, respectively. In summary, Se supplementation alleviated the negative impact of HS on IPEC-J2 cells, and their cellular protective effect was associated with regulation expression of selenoproteins, and SeMet exhibited a better protective effect.

The emergence of antimicrobial resistance raises serious concerns worldwide. Probiotics offer a promising alternative to enhance growth promotion in farm animals; however, their mode of action still needs to be elucidated. The IPEC-J2 cell line (porcine intestinal epithelial cells) is an appropriate tool to study the effect of probiotics on intestinal epithelial cells. In our experiments, IPEC-J2 cells were challenged by two gastrointestinal (GI) infection causing agents, Escherichia coli (E. coli) or Salmonella enterica ser. Typhimurium (S. Typhimurium). We focused on determining the effect of pre-, co-, and post-treatment with two probiotic candidates, Bacillus licheniformis or Bacillus subtilis, on the barrier function, proinflammatory cytokine (IL-6 and IL-8) response, and intracellular reactive oxygen species (ROS) production of IPEC-J2 cells, in addition to the adhesion inhibition effect. Bacillus licheniformis (B. licheniformis) and Bacillus subtilis (B. subtilis) proved to be anti-inflammatory and had an antioxidant effect under certain treatment combinations, and further effectively inhibited the adhesion of pathogenic bacteria. Interestingly, they had little effect on paracellular permeability. Based on our results, Bacillus licheniformis and Bacillus subtilis are both promising candidates to contribute to the beneficial effects of probiotic multispecies mixtures.

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.

The accumulation of reactive oxygen species (ROS) triggers oxidative stress in cells by oxidizing and modifying various cellular components, preventing them from performing their inherent functions, ultimately leading to apoptosis and autophagy. Glutathione (GSH) is a ubiquitous intracellular peptide with multiple functions. In this study, a hydrogen peroxide (H2O2)-induced oxidative damage model in IPEC-J2 cells was used to investigate the cellular protection mechanism of exogenous GSH against oxidative stress. The results showed that GSH supplement improved the cell viability reduced by H2O2-induced oxidative damage model in IPEC-J2 cells in a dose-dependent manner. Moreover, supplement with GSH also attenuated the H2O2-induced MMP loss, and effectively decreased the H2O2-induced mitochondrial dysfunction by increasing the content of mtDNA and upregulating the expression TFAM. Exogenous GSH treatment significantly decreased the ROS and MDA levels, improved SOD activity in H2O2-treated cells and reduced H2O2-induced early apoptosis in IPEC-J2 cells. This study showed that exogenous GSH can protect IPEC-J2 cells against apoptosis induced by oxidative stress through mitochondrial mechanisms.