PI3K/Akt signaling pathway mediates the effect of low-dose boron on barrier function, proliferation and apoptosis in rat intestinal epithelial cells.

Boron is an essential trace element with roles in growth, development, and physiological functions; however, its mechanism of action is still unclear. In this study, the regulatory roles of the PI3K/Akt signaling pathway on boron-induced changes in barrier function, proliferation, and apoptosis in rat intestinal epithelial cells were evaluated. Occludin levels, the proportion of cells in the G2/M phase, cell proliferation rate, and mRNA and protein expression levels of PCNA were higher, while the proportions of cells in the G0/G1 and S phases, apoptosis rate, and caspase-3 mRNA and protein expression levels were lower in cells treated with 0.8 mmol/L boron than in control IEC-6 cells (P < 0.01 or P < 0.05). However, 40 mmol/L boron decreased ZO-1 and Occludin levels, the proportion of cells in the G2/M phase, cell proliferation rate, and mRNA and protein levels of PCNA and increased the apoptosis rate and caspase-3 mRNA expression (P < 0.01 or P < 0.05). After specifically blocking PI3K and Akt signals (using LY294002 and MK-2206 2HCL), 0.8 mmol/L boron had no effects on Occludin, PCNA level, apoptosis rates, and caspase-3 levels (P < 0.05); however, the proliferation rate and PCNA levels decreased significantly (P < 0.01 or P < 0.05). The addition of 40 mmol/L boron did not affect ZO-1 and Occludin levels and did not affect the apoptosis rate or PCNA and caspase-3 levels. These results suggested that the PI3K/Akt signaling pathway mediates the effects of low-dose boron on IEC-6 cells.

From inflammation to pyroptosis: Understanding the consequences of cadmium exposure in chicken liver cells.

Hepatotoxicity is frequently observed following acute cadmium (Cd) exposure in chicken. Oxidative stress and subsequent inflammation are regarded as the main reasons for cadmium-induced liver injury. NOD-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome-induced pyroptosis is involved in various inflammatory diseases, including liver injury. Poultry are more susceptible to harmful effects of heavy metals. However, the mechanism of cadmium-induced liver injury in chicken is still elusive. In this study, the effect of cadmium on chicken liver cells and the underlying mechanisms were investigated. The results showed mitochondria was damaged and excessive reactive oxygen species (ROS) were generated in chicken liver cell line LMH after cadmium exposure. Furthermore, cadmium-induced NLRP3 inflammasome activation and the cell membrane rupture indicated LMH cells pyroptosis. The ROS scavengers, acetylcysteine (NAC) and Mito-TEMPO prevented pyroptosis in LMH cells, suggesting that ROS were responsible for the activation of the NLRP3 inflammasome induced by cadmium. Additionally, anti-oxidative transcription factor Nrf2 was inhibited after cadmium exposure, explaining the excessive ROS generation. In summary, our study showed that cadmium leads to ROS generation by inducing mitochondrial damage and inhibiting Nrf2 activity, which promotes NLRP3 inflammasome activation and eventually induces pyroptosis in LMH cells.

New insights into the unfolded protein response (UPR)-anterior gradient 2 (AGR2) pathway in the regulation of intestinal barrier function in weaned piglets.

Sustained dysfunction of the intestinal barrier caused by early weaning is a major factor that induces postweaning diarrhea in weaned piglets. In both healthy and diseased states, the intestinal barrier is regulated by goblet cells. Alterations in the characteristics of goblet cells are linked to intestinal barrier dysfunction and inflammatory conditions during pathogenic infections. In this review, we summarize the current understanding of the mechanisms of the unfolded protein response (UPR) and anterior gradient 2 (AGR2) in maintaining intestinal barrier function and how modifications to these systems affect mucus barrier characteristics and goblet cell dysregulation. We highlight a novel mechanism underlying the UPR-AGR2 pathway, which affects goblet cell differentiation and maturation and the synthesis and secretion of mucin by regulating epidermal growth factor receptor and mucin 2. This study provides a theoretical basis and new insights into the regulation of intestinal health in weaned piglets.

MAPK Signaling Pathway Plays Different Regulatory Roles in the Effects of Boric Acid on Proliferation, Apoptosis, and Immune Function of Splenic Lymphocytes in Rats.

Boron is one of the essential trace elements in animals. Although boron supplementation can enhance immune function and promote cell proliferation, high-dose boron supplementation can negatively affect immune function and inhibit cell proliferation. Furthermore, its action pathway is unknown. In this study, ERK1/2, JNK, and p38MAPK signaling pathways were blocked using specific blockers to investigate the impact of low-dose and high-dose boron on proliferation, apoptosis, and immune function of lymphocytes, and the expression of genes related to cell proliferation and apoptosis in rats. The addition of 0.4 mmol/L boron did not affect the ratio of CD4+/CD8+ T cells (P>0.05), IgG and IFN-γ contents (P>0.05), the proliferation rate of lymphocytes (P>0.05), and mRNA and protein expressions of PCNA (P>0.05) in the spleen after ERK1/2 signal pathway was selectively inhibited. Moreover, the addition of 40 mmol/L boron did not affect the proportion of CD4+ T cells, contents of IgG and cytokines (IL-2 and IL-4), proliferation and apoptosis rates of lymphocytes, and expression of proliferation- and apoptosis-related genes in the spleen. Meanwhile, the addition of 0.4 mmol/l boron increased the ratio of CD4+/CD8+ T cells (P<0.05 or P<0.01), IFN-γ or IgG contents (P<0.05), and the proliferation rate of lymphocytes (P<0.05) in spleen after selective inhibition of JNK or p38MAPK signaling pathways, while the protein expression of Caspase-3 decreased (P<0.05 or P<0.01). Furthermore, 40 mmol/L boron decreased the proportion of lymphocyte subsets, cytokine contents, proliferation rate of lymphocytes, and mRNA and protein expressions of PCNA. In contrast, the mRNA and protein expressions of Caspase-3 and protein expression of Bax were increased. These results indicate that ERK1/2 signaling pathway mainly regulates the effects of low-dose and high-dose boron on proliferation, apoptosis, and immune function of splenic lymphocytes.

Proteomic Analysis of Rat Duodenum Reveals the Modulatory Effect of Boron Supplementation on Immune Activity.

The proper supplementation of boron, an essential trace element, can enhance animal immune function. We utilized the method of TMT peptide labeling in conjunction with LC-MS/MS quantitative proteomics for the purpose of examining the effects of boric acid on a rat model and analyzing proteins from the duodenum. In total, 5594 proteins were obtained from the 0, 10, and 320 mg/L boron treatment groups. Two hundred eighty-four proteins that exhibit differential expression were detected. Among the comparison, groups of 0 vs. 10 mg/L, 0 vs. 320 mg/L, and 10 vs. 320 mg/L of boron, 110, 32, and 179 proteins, respectively, demonstrated differential expression. The results revealed that these differential expression proteins (DEPs) mainly clustered into two profiles. GO annotations suggested that most of the DEPs played a role in the immune system process, in which 2'-5'-oligoadenylate synthetase-like, myxovirus resistance 1, myxovirus resistance 2, dynein cytoplasmic 1 intermediate chain 1, and coiled-coil domain containing 88B showed differential expression. The DEPs had demonstrated an augmentation in the signaling pathways, which primarily include phagosome, antigen processing, and presentation, as well as cell adhesion molecules (CAMs). Our study found that immune responses in the duodenum were enhanced by lower doses of boron and that this effect is likely mediated by changes in protein expression patterns in related signaling pathways. It offers an in-depth understanding of the underlying molecular mechanisms that lead to immune modulation in rats subjected to dietary boron treatment.

Transcriptomic Profiling of Meat Quality Traits of Skeletal Muscles of the Chinese Indigenous Huai Pig and Duroc Pig.

The Huai pig is a well-known indigenous pig breed in China. The main advantages of Huai pigs over Western commercial pig breeds include a high intramuscular fat (IMF) content and good meat quality. There are significant differences in the meat quality traits of the same muscle part or different muscle parts of the same variety. To investigate the potential genetic mechanism underlying the meat quality differences in different pig breeds or muscle groups, longissimus dorsi (LD), psoas major (PM), and biceps femoris (BF) muscle tissues were collected from two pig breeds (Huai and Duroc). There were significant differences in meat quality traits and amino acid content. We assessed the muscle transcriptomic profiles using high-throughput RNA sequencing. The IMF content in the LD, PM, and BF muscles of Huai pigs was significantly higher than that in Duroc pigs (p < 0.05). Similarly, the content of flavor amino acids in the three muscle groups was significantly higher in Huai pigs than that in Duroc pigs (p < 0.05). We identified 175, 110, and 86 differentially expressed genes (DEGs) between the LD, PM, and BF muscles of the Huai and Duroc pigs, respectively. The DEGs of the different pig breeds and muscle regions were significantly enriched in the biological processes and signaling pathways related to muscle fiber type, IMF deposition, lipid metabolism, PPAR signaling, cAMP signaling, amino acid metabolism, and ECM-receptor interaction. Our findings might help improve pork yield by using the obtained DEGs for marker-assisted selection and providing a theoretical reference for evaluating and improving pork quality.

Ionomics-metabolome association analysis as a new approach to the impact of dietary copper levels in suckling piglets model.

Ionomics-metabolomics association analysis is a novel method to elucidating the potential mechanisms underlying the effects of dietary copper on the overall health parameters of suckling piglets model. Few studies have elucidated the relationship between the changes of ionic and metabolic homeostasis responses to dietary copper level. The growth performance data was obtained from 180 suckling piglets which access to different copper levels: 6 (low copper diet, LC), 20 (control diet, CON), and 300 (high copper diet, HC) mg·kg-1 copper (based on diet, supplementation from CuSO4), and offered ad libitum from d 14 until weaning at 40 d of age. Dietary high level copper (300 mg·kg-1) increased the ADG and ADFI during d 14 to 28 of piglets. Six elements (Mg, Na, K, P, Cu, and Mn) concentrations significantly changes in hair among the three treatment diets. The significant increased concentrations of Na and K, and decreased concentration of Mg and Mn in 300 mg·kg-1 than 20 mg·kg-1 copper diet was observed. In current study, with the increase in copper level from 20 to 300 mg·kg-1 in diet, the correlation between hair Na, K and Cu, Mn, Zn vanish. Hair Na and K were positively correlated with serum total antioxidant capacity (T-AOC) and negatively correlated with tumor necrosis factor-α (TNF-α). The hair Cu was negatively correlated with serum malondialdehyde (MDA), total bile acid (TBA). The fecal Cu was positively correlated with serum growth hormone (GH). The results suggested that the average daily gain (ADG) in 6 mg·kg-1 copper diet and the average daily feed intake (ADFI) in 20 mg·kg-1 copper diet were decreased than 300 mg·kg-1 copper diet during d 14 to 28 and the ADG was decreased in 6 and 20 mg·kg-1 copper diets in d 29 to 40 of piglets. Dietary 20 mg·kg-1 copper maintain ion homeostasis due to increase the number of positive correlations between macroelements-microelements in hair and serum. Significantly changed Na, K, Mg, Mn and Cu concentrations in hair can reflect the adverse effects of dietary 300 mg·kg-1 copper of suckling piglets. We believe our results may benefit people to gain a better understanding of the ion interactions and metabolic homeostasis of heavy metal elements that are critical to human and animal health.

Hericium erinaceus polysaccharide improves the microstructure, immune function, proliferation and reduces apoptosis of thymus and spleen tissue cells of immunosuppressed mice.

In order to study the effect of Hericium erinaceus polysaccharide (HEP) on the immune and antioxidation functions of immunosuppressed mice. The control group received distilled water orally and the model and experimental groups I, II, and III received 0, 80, 160, and 320 mg/kg HEP respectively for a fortnight after re-molding with cyoclphosphnalide (CTX). Compared with the control group, the secretion of IL-2, IL-4, and IFN-γ, the activity or content of T-AOC, T-SOD, and GSH-PX, and the expression of PCNA mRNA in the thymus and spleen were reduced in immunosuppressed mice (P < .05 or P < .01). Compared with immunosuppressed mice, the levels of IL-2, IFN-γ, and GSH-PX and the PCNA mRNA expression of spleen and thymus were increased (P < .05 or P < .01), and the microstructure were also obviously improved in the experimental group III. Overall, 320 mg/kg of HEP significantly improved the immune and antioxidant functions.

Role of gga-miR-29b-3p in suppressing the proliferation, invasion and migration of MSB1 Marek's disease tumor cells by the targeting of the DNMT3B gene.

Background: Marek's disease (MD), a class II infectious, lymphoproliferative disease that mainly afflicts poultry, has been shown to cause wasting, limb paralysis, and often acute death. It is a neoplastic disease caused by a cell-binding herpesvirus that leads to the formation of tumors in various organs and tissues. Our previous reports have found that the microRNA, gga-miR-29b-3p, showed abnormal expression in MD lymphoma. However, it remains unknown whether gga-miR-29b-3p affects MD tumorigenesis. Methods: The MD tumor cell line MSB1 was chosen to analyze the characteristics of gga-miR-29b-3p in tumors. Cell proliferation and migration were assessed by Cell Counting Kit-8 (CCK-8) and Transwell, respectively, and cell apoptosis and cycle were analyzed via fluorescent staining and flow cytometry, respectively. The regulation between gga-miR-29b-3p and its potential target genes was verified by dual luciferase results and loss-of-function assays. The effect of target genes was verified by examining the degree of RNA interference on MSB1 cells. Results: Analysis revealed that gga-miR-29b-3p impaired the proliferation of the MSB1 MD tumor cell line, induced apoptosis without obvious effects on the cell cycle, and suppressed the expression of the invasion-associated MMP2 and MMP9 genes. It was concluded that DNMT3B is the direct target of gga-miR-29b-3p. As expected, the effects of DNMT3B knockdown with small interfering RNA (siRNA) on MSB1 cell proliferation, apoptosis, and cycle were associated with gga-miR-29b-3p overexpression. Moreover, BCL2 and BCL2L1 were downregulated and TNFSF10 was upregulated in both the gga-miR-29b-3p overexpression and DNMT3B knockdown groups. The expression levels of invasion-related genes were decreased post-DNMT3B knockdown. In both the gga-miR-29b-3p overexpression and DNMT3B knockdown conditions, a decrease in MEQ oncogene expression in MD virus was observed. Conclusions: Overall, gga-miR-29b-3p was demonstrated to have a suppressive effect in MD lymphoma progression via the targeting of the DNMT3B gene. Gga-miR-29b-3p overexpression and DNMT3B knockdown inhibited MSB1 cell proliferation through suppressing the pro-apoptotic gene expression and elevating the anti-apoptotic gene expression in the apoptosis pathway. Our study provides a theoretical basis for targeted treatment of MD.

Effect of Dietary Fructus mume and Scutellaria baicalensis Georgi on the Fecal Microbiota and Its Correlation with Apparent Nutrient Digestibility in Weaned Piglets.

Traditional Chinese medicine (TCM) has long been demonstrated to exert a therapeutic effect on various diseases and has been used as a substitute for antibiotics in pig production. However, few studies have investigated the relationship between the intestinal microbiota and apparent nutrient digestibility when weaned piglet diets are supplemented with TCM. One hundred and sixty-two 25-day-old weaning piglets were housed in an environmentally controlled nursery facility and fed a basal diet (control group, n = 54) or a TCM complex (Fructus mume 1%, Scutellaria baicalensis Georgi 3%) (TCM group, n = 54), or a fermented diet with a complex of these two TCMs (F-TCM group, n = 54). Compared with the control group, in the TCM and F-TCM groups, the average daily gain (ADG) increased (p < 0.05), the F:G ratio and diarrhea rate decreased (p < 0.05), and the apparent digestibility of dry matter (DM) and ether extract (EE) of weaned piglets increased (p < 0.05). Bacteroidetes and Firmicutes were the predominant phyla, representing approximately 95% of all sequences. The abundance of four genera and 10 OTUs (belonging to Ruminococcaceae_UCG-014, Lachnoclostridium, Prevotellaceae_NK3B31 group, Prevotella_1) were negatively correlated with apparent EE digestibility (p < 0.05). The results suggest that weaned piglets fed with antibiotic-free diets supplemented with Fructus mume and Scutellaria baicalensis Georgi gained more weight and were healthier. When added to the diet, the complex of these two TCMs may have a direct impact on apparent EE digestibility by modifying the gut microbial composition, which favors the health of weaned piglets.

Sodium selenite attenuates zearalenone-induced apoptosis through inhibition of endoplasmic reticulum stress in goat trophoblast cells.

Zearalenone (ZEL)-induced apoptosis in different cells is mediated by various molecular mechanisms, including endoplasmic reticulum (ER) stress. Selenium, an inorganic micronutrient, has several cytoprotective properties, but its potential protective action against ZEL-induced apoptosis in trophoblast cells and the precise mechanisms remain unclear. In this study, we investigated the effects of sodium selenite, a predominant chemical form of selenium, on cell viability, apoptosis, and progesterone (P4) production in ZEL-treated goat trophoblast cell line and explored the underlying molecular mechanisms. ZEL treatment repressed cell viability and promoted apoptosis, which was accompanied by an enhancement of the activity of caspase 3, a key executioner of apoptosis. ZEL treatment was involved in the upregulation of malonaldehyde (MDA) levels and was implicated in the reduction of the protein expression of selenoprotein S (SELS), thereby triggering protein expression of ER stress biomarkers (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP)). However, sodium selenite attenuates these adverse effects, including increases in apoptotic rate, caspase 3 activity, MDA, GRP78, and CHOP expression and decreases in SELS expression in cells treated with ZEL or Thapsigargin (Tg, an ER stress agonist). Simultaneously, 4-phenylbutyric acid (4-PBA, an ER stress antagonist) treatment significantly alleviated the ZEL-induced deleterious effects on cells in response to ZEL, similarly to sodium selenite. In addition, sodium selenite supplementation effectively rescued the ZEL-induced decrease in P4 production in ZEL-treated cells. In summary, these findings suggest that ZEL triggers apoptosis in goat trophoblast cells by downregulating SELS expression and activating the ER stress signaling pathway and that sodium selenite protects against these detrimental effects. This study provides novel insights into the benefits of using selenium against ZEL-induced apoptosis and cellular damage.

Transcriptome Profiling of Duodenum Reveals the Importance of Boron Supplementation in Modulating Immune Activities in Rats.

As an essential trace element, appropriate boron supplementation can promote immune function of animals. To illustrate the effects of boron in a rat model, RNA-Seq was conducted for the RNA from duodenum after treatment with different concentration of boron in which boron was given in the form of boric acid. More than 47 million reads were obtained in 0, 10, and 320 mg/L boron (0, 57.21, and 1830.66 mg/L boric acid) treatment groups that produced 58 965 402, 48 607 328, and 46 760 660 clean reads, respectively. More than 95% of the clean reads were successfully matched to the rat reference genome and assembled to generate 32 662 transcripts. A total of 624 and 391 differentially expressed candidate genes (DEGs) were found between 0 vs.10 and 0 vs. 320 mg/L boron comparison groups. We also identified transcription start site, transcription terminal site, and skipped exons as the main alternative splicing events. GO annotations revealed most of DEGs were involved in the regulation of immune activity. The DEGs were enriched in influenza A, herpes simplex infection, cytosolic DNA-sensing pathway, and antigen processing and presentation signaling pathways. The expression levels of genes enriched in these signaling pathways indicate that lower doses of boron could achieve better effects on promoting immune response in the duodenum. These effects on the immune system appear to be mediated via altering the expression patterns of genes involved in the related signaling pathways in a dose-dependent pattern. These data provide more insights into the molecular mechanisms of immune regulation in rats in response to dietary boron treatment.

Effect of Boron on Microstructure, Immune Function, Expression of Tight Junction Protein, Cell Proliferation and Apoptosis of Duodenum in Rats.

Boron is an essential trace element for animals. Appropriate boron supplementation can produce beneficial effects on the animal body, while a high dose of boron has adverse and even toxic effects. Our aim was to investigate the impact of different doses of boron on the microstructure of duodenum in rats, expression of secretory immunoglobulin A (SIgA) and tight junction protein, cell proliferation and apoptosis. Eighty newly weaned clean Sprague-Dawley (SD) rats were given distilled water supplemented with 0, 10, 20, 40, 80, 160, 320, and 640 mg/L of boron for 60 days. We found that supplementation of 40 and 80 mg/L boron could increase the height of duodenal villi and the crypt depth, the number of intraepithelial lymphocytes (IELs) and goblet cells, the expression of SIgA, Zonula occludens-1 (ZO-1) and occludin, and proliferating cell nuclear antigen (PCNA) in duodenum of rats; decrease expression of Caspase-3 mRNA and the number of Caspase-3-positive cells, but supplementation of 320 and 640 mg/L boron could have the opposite effect in these indexes. The results showed that supplemented with 40 and 80 mg/L of boron could improve the structure and function of duodenum, while supplemented with 320-640 mg/L had a significant inhibitory effect.

Boron Attenuates Heat Stress-Induced Apoptosis by Inhibiting Endoplasmic Reticulum Stress in Mouse Granulosa Cells.

Heat stress-induced apoptosis in granulosa cells is mediated by multiple apoptotic signaling pathways, including endoplasmic reticulum (ER) stress. Boron is a naturally occurring trace element with several cytoprotective properties. Nonetheless, the molecular mechanisms involved in the protective functions of boron in granulosa cells undergoing apoptosis caused by heat stress (HS) remain unclear. In this study, we investigated the role of boric acid, a predominant chemical form of boron, in HS-induced apoptotic damage in mouse granulosa cells (mGCs) and explored the underlying mechanisms. We found that HS treatment suppressed cell viability; increased the apoptotic rate of cells; potentiated the activity of caspase-3, a key player in the caspase-mediated apoptotic signaling pathway; and activated ER stress markers, including glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) in mGCs. However, boric acid treatment effectively alleviated the effects of both HS-induced and thapsigargin (an ER stress agonist)-induced apoptosis, such as the enhanced activity of caspase-3 and increase in GRP78 and CHOP expression. Moreover, treatment with 4-phenylbutyrate (4-PBA), an ER stress antagonist, significantly attenuated these HS-induced adverse effects in mGCs. In addition, boric acid supplementation in the culture medium significantly restored the decreased estradiol levels in heat-treated mGCs. The administration of boric acid to female mice previously exposed to hyperthermal conditions effectively restored the levels of serum estradiol in vivo. Collectively, these findings suggest that HS induces apoptosis in mGCs via ER stress pathways and that boron has a protective effect against these adverse effects. This study provides novel insights into the benefits of using boron against heat-induced apoptosis.

GPR30 mediated effects of boron on rat spleen lymphocyte proliferation, apoptosis, and immune function.

Supplementing different quantities of boron can significantly affect immune function in rat spleen, but the mechanism of action behind this effect remains unclear. Our purpose was to study the involvement of the estrogen membrane receptor GPR30 in the effect of boron on the proliferation, apoptosis, and immune function of rat spleen lymphocytes. Results showed that the addition of 0.4 mmol/L boron had a beneficial effect on the immune function and proliferation of spleen lymphocytes, but the addition of 40 mmol/L boron had opposite effect. After using G-15 to selectively inhibit GPR30, the proportions of CD4+ and CD8+ T cells, the content of IL-2 and IFN-γ, and the expression of PCNA protein were significantly decreased, while lymphocyte apoptosis rate increased significantly (p < 0.05 or p < 0.01). After G-15 treatment, the addition of 0.4 mmol/L boron had no effects on T cell subsets, lymphocyte proliferation, PCNA protein expression, and IgG and cytokine content (P > 0.05), while the addition of 40 mmol/L boron did not change the effects on lymphocyte subsets, proliferation and apoptosis. The results suggested that GPR30 mediates the effects of 0.4 mmol/L boron boron on the proliferation, apoptosis and immune function of spleen lymphocytes.

Selenium Attenuates Chronic Heat Stress-Induced Apoptosis via the Inhibition of Endoplasmic Reticulum Stress in Mouse Granulosa Cells.

Heat stress induces apoptosis in various cells. Selenium, an essential micronutrient, has beneficial effects in maintaining the cellular physiological functions. However, its potential protective action against chronic heat stress (CHS)-induced apoptosis in granulosa cells and the related molecular mechanisms are not fully elucidated. In this study, we investigated the roles of selenium in CHS-induced apoptosis in mouse granulosa cells and explored its underlying mechanism. The heat treatment for 6-48 h induced apoptosis, potentiated caspase 3 activity, increased the expression levels of apoptosis-related gene BAX and ER stress markers, glucose-regulated protein 78 (GRP78), and CCAAT/enhancer binding protein homologous protein (CHOP) in mouse granulosa cells. The treatment with ER stress inhibitor 4-PBA significantly attenuated the adverse effects caused by CHS. Selenium treatment significantly attenuated the CHS- or thapsigargin (Tg, an ER stress activator)-induced apoptosis, potentiation of caspase 3 activity, and the increased protein expression levels of BAX, GRP78, and CHOP. Additionally, treatment of the cells with 5 ng/mL selenium significantly ameliorated the levels of estradiol, which were decreased in response to heat exposure. Consistently, administering selenium supplement alleviated the hyperthermia-caused reduction in the serum estradiol levels in vivo. Together, our findings indicate that selenium has protective effects on CHS-induced apoptosis via inhibition of the ER stress pathway. The current study provides new insights in understanding the role of selenium during the process of heat-induced cell apoptosis.

Effects of Boron on Cytotoxicity, Apoptosis, and Cell Cycle of Cultured Rat Sertoli Cells In vitro.

The present study aimed to investigate the effects of the administration of boron on viability, apoptosis, and cell cycle of primary rat Sertoli cells (SCs) in vitro. SCs were aseptically isolated from 18-22-day-old male Sprague-Dawley (SD) rats. SCs were identified with immunofluorescence using anti-vimentin antibody. Further, to investigate the effects of boron on Sertoli cells, SCs of the boron treatment group were exposed to different concentrations (0.25, 0.5, 1, 5, 10, 40, and 80 mmol/L) of boric acid. Using MTT and Cell Counting Kit-8 assays, the impact of boron on SCs viability was analyzed. Cell apoptosis and cycle of SCs were analyzed using flow cytometry. A concentration of 0.5 mmol/L boric acid resulted in the highest viability and lowest necrosis and apoptosis. Above this concentration (even 1.0 mmol/L) showed lower viability and higher levels of necrosis and apoptosis. Administration of < 0.5 mmol/L boron significantly promoted the viability of Sertoli cells (P < 0.01); however, the exposure to high dose (> 10 mmol/L) of boron exhibited significant adverse effects on Sertoli cells (P < 0.01) and even toxic effects, inhibiting cell viability compared to the control group. Flow cytometry analysis showed that treatment with 0.5 mmol/L of boron significantly inhibited the apoptosis of Sertoli cells and the proportion of cells in S and G2/M phases was markedly increased; however, a higher concentration of 40 and 80 mmol/L of boron promoted Sertoli cell apoptosis and cells were completely arrested at G0/G1 phase. Boron at doses below 0.5 mmol/L could significantly improve the viable capacity of testicular Sertoli cells in vitro and inhibit their apoptosis. However, high dose of boron (at a concentration higher than 5.0 mmol/L) exhibited noticeable toxic effects, inhibiting cell viability, accelerating apoptosis of Sertoli cells, and arresting cell cycle at G0/G1 phase.

Isoleucine attenuates infection induced by E. coli challenge through the modulation of intestinal endogenous antimicrobial peptide expression and the inhibition of the increase in plasma endotoxin and IL-6 in weaned pigs.

Enteric infection is a major cause of morbidity and mortality in both humans and animals worldwide. Immunotherapy against intestinal infection is a well-known alternative to the antibiotic strategy. Herein, we demonstrated that isoleucine significantly suppressed the multiplication of E. coli in the presence of IPEC-J2 cells. Isoleucine supplementation enhanced the concentrations of total plasma protein and IgA in pigs compared to the alanine control diet, while inhibiting the increase in plasma endotoxin and IL-6 contents induced by E. coli challenge. A significant interaction between the E. coli challenge and the diet treatment was found in the red blood cell volume. Isoleucine improved the expression of porcine ß-defensin-1 (pBD-1), pBD-2, pBD-3, pBD-114 and pBD-129 in the jejunum and ileum of pigs with or without E. coli challenge. Conclusively, isoleucine attenuated the infection caused by the E. coli challenge possibly through increasing the intestinal ß-defensin expression and inhibiting the increase in plasma endotoxin and IL-6 in weaned pigs.

Correction: Isoleucine attenuates infection induced by E. coli challenge through the modulation of intestinal endogenous antimicrobial peptide expression and the inhibition of the increase in plasma endotoxin and IL-6 in weaned pigs.

Correction for 'Isoleucine attenuates infection induced by E. coli challenge through the modulation of intestinal endogenous antimicrobial peptide expression and the inhibition of the increase in plasma endotoxin and IL-6 in weaned pigs' by Man Ren et al., Food Funct., 2019, DOI: 10.1039/c9fo00218a.

Effects of Selenium Yeast in Combination with Boron on Muscle Growth and Muscle Quality in Broilers.

The effect of selenium yeast in combination with boron on both growth and quality of the muscle in broilers was investigated. A total of 600 one-day-old Arbor Acres broilers were randomly divided into five groups with 120 broilers per group (6 replicates per group). The control group received a basal diet, and experimental groups I-IV received the same basal diet supplemented with 0.3 mg/kg selenium yeast and different doses of boron (0, 5, 10, and 15 mg/kg, respectively). The experiment was conducted for 42 days. Breast and thigh muscles were harvested and muscle quality were examined on day 21 and day 42 of the experiment. Compared to the control group, at 21 days of age, the thigh muscle weight and index were significantly increased in broilers of experimental group II (all P < 0.05); however, the drip loss and shear force of breast and thigh muscle were significantly decreased (P < 0.05). At 42 days of age, the breast muscle weight and index as well as the breast and thigh muscle water holding capability had significantly increased in broilers of experimental group II (all P < 0.05); the breast and thigh muscle drip loss, cooking loss and shear force, and thigh muscle fiber diameter were significantly reduced (all P < 0.05). Breast and thigh muscle fibers were tightly arranged with small cross-sectional areas in broilers of experimental group II. These results suggest that supplementation of 0.3 mg/kg selenium yeast in combination with 5 mg/kg boron in the basal diet can promote muscle growth and improved muscle quality in broilers.