Selenium-enriched peptides identified from selenium-enriched soybean protein hydrolysate: protective effects against heat damage in Caco-2 cells.

Our previous study evaluated the antioxidant and anti-inflammatory activities of selenium-enriched soybean peptides (SePPs) in vivo. In this study, we purified SePPs via gel filtration chromatography and obtained five fractions (F1, F2, F3, F4 and F5), among which F3 displayed the highest antioxidant and anti-inflammatory activities. Nineteen selenium-enriched peptides were identified in F3 by mass spectrometry. Two selenium-enriched peptides with sequences ESeCQIQKL (Sep-1) and SELRSPKSeC (Sep-2) were selected for synthesis based on their score and the number of hydrophobic amino acids, acidic and basic amino acids. Both Sep-1 and Sep-2 exhibited preventive effects on the heat stress-induced impairment of intestinal epithelial cell integrity, oxidative stress and inflammatory responses in a Caco-2 cell model. Pretreatment of the cells with Sep-1 or Sep-2 for 24 h reduced intracellular reactive oxygen species (ROS) generation, prevented the disruption of tight junction (TJ) proteins, and decreased paracellular permeability. Western blot results showed that Sep-1 and Sep-2 could improve the abnormal expressions of Nrf2, Keap1, NLRP3, caspase-1 and ASC/TMS1, thereby enhancing the glutathione (GSH) redox system and reducing IL-1ß and IL-18 concentrations. Sep-1 activated the Nrf2-Keap1 signaling pathway significantly more than Sep-2. Molecular docking results indicated that Sep-1 and Sep-2 are both bound to Keap1 and NLRP3 in the form of hydrogen bonds, hydrophobic interactions and salt bridges, which interferes with Nrf2 and NLRP3 signaling. Molecular dynamics simulations suggested that more hydrogen bonds were formed during the resultant process of Sep-1 with Keap1, and the compactness and stability of the complex structure were better than those of Sep-2. These findings confirm the value of both Sep-1 and Sep-2 in the development of dietary supplements as potential alternatives for heat damage and related disease prevention.

Selenium-Enriched Soybean Peptides as Novel Organic Selenium Compound Supplements: Inhibition of Occupational Air Pollution Exposure-Induced Apoptosis in Lung Epithelial Cells.

The occupational groups exposed to air pollutants, particularly PM2.5, are closely linked to the initiation and advancement of respiratory disorders. The aim of this study is to investigate the potential protective properties of selenium-enriched soybean peptides (Se-SPeps), a novel Se supplement, in mitigating apoptosis triggered by PM2.5 in A549 lung epithelial cells. The results indicate a concentration-dependent reduction in the viability of A549 cells caused by PM2.5, while Se-SPeps at concentrations of 62.5-500 µg/mL showed no significant effect. Additionally, the Se-SPeps reduced the production of ROS, proinflammatory cytokines, and apoptosis in response to PM2.5 exposure. The Se-SPeps suppressed the PM2.5-induced upregulation of Bax/Bcl-2 and caspase-3, while also restoring reductions in p-Akt in A549 cells. The antiapoptotic effects of Se-SPeps have been found to be more effective compared to SPeps, SeMet, and Na2SeO3 when evaluated at an equivalent protein or Se concentration. Our study results furnish evidence that supports the role of Se-SPeps in reducing the harmful effects of PM2.5, particularly in relation to its effect on apoptosis, oxidative stress, and inflammation.

The Formation, Structural Characteristics, Absorption Pathways and Bioavailability of Calcium-Peptide Chelates.

Calcium is one of the most important mineral elements in the human body and is closely related to the maintenance of human health. To prevent calcium deficiency, various calcium supplements have been developed, but their application tends to be limited by low calcium content and highly irritating effects on the stomach, among other side effects. Recently, calcium-peptide chelates, which have excellent stability and are easily absorbed, have received attention as an alternative emerging calcium supplement. Calcium-binding peptides (CaBP) are usually obtained via the hydrolysis of animal or plant proteins, and calcium-binding capacity (CaBC) can be further improved through chromatographic purification techniques. In calcium ions, the phosphate group, carboxylic group and nitrogen atom in the peptide are the main binding sites, and the four modes of combination are the unidentate mode, bidentate mode, bridging mode and α mode. The stability and safety of calcium-peptide chelates are discussed in this paper, the intestinal absorption pathways of calcium elements and peptides are described, and the bioavailability of calcium-peptide chelates, both in vitro and in vivo, is also introduced. This review of the research status of calcium-peptide chelates aims to provide a reasonable theoretical basis for their application as calcium supplementation products.

Selenium-enriched soybean peptides pretreatment attenuates lung injury in mice induced by fine particulate matters (PM2.5) through inhibition of TLR4/NF-κB/IκBα signaling pathway and inflammasome generation.

This study aimed to identify and prepare peptides from selenium (Se)-enriched soybeans and determine whether dietary Se-enriched soybean peptides (Se-SPep) could inhibit lung injury in mice induced by fine particulate matter 2.5 (PM2.5). BALB/c mice were randomly divided into six groups. The mice in the prevention groups were pretreated with 378 mg kg-1 of Se-SPep, soybean peptides (SPep), and Se-enriched soybean protein (Se-SPro), respectively, for four weeks. The mice in the PM2.5 exposure group received concentrated PM2.5 (15 µg per day mice) for 1 h daily from the third week for two weeks. The results showed that the leukocyte and cytokine (IL-1ß, IL-6, TNF-α) levels in the bronchoalveolar lavage fluid (BALF) of the PM2.5 exposure group were higher than those in the control group. Se-SPep pretreatment decreased the IL-1ß, IL-6, and TNF-α levels compared with the PM2.5 exposure group. Additionally, Se-SPep pretreatment inhibited TLR4/NF-κB/IκBα and NLRP3/ASC/caspase-1 protein expression in the lungs. In conclusion, Se-SPep pretreatment may protect the lungs of the mice against PM2.5-induced inflammation, suggesting that Se-SPep represents a potential preventative agent to inhibit PM2.5-induced lung injury.

The adverse effect of heat stress and potential nutritional interventions.

Heat stress can cause tissue damage and metabolic disturbances, including intestinal and liver dysfunction, acid-base imbalance, oxidative damage, inflammatory response, and immune suppression. Serious cases can lead to heatstroke, which can be life-threatening. The body often finds it challenging to counteract these adverse effects, and traditional cooling methods are limited by the inconvenience of tool portability and the difficulty of determining the cooling endpoint. Consequently, more research was conducted to prevent and mitigate the negative effect of heat stress via nutritional intervention. This article reviewed the pathological changes and altered metabolic mechanisms caused by heat stress and discussed the protein (amino acid), vitamin, trace element, and electrolyte action pathways and mechanisms to mitigate heat stress and prevent heat-related disease. The main food sources for these nutrients and the recommended micronutrient supplementation forms were summarized to provide scientific dietary protocols for special populations.

A Comprehensive Comparison of Different Selenium Supplements: Mitigation of Heat Stress and Exercise Fatigue-Induced Liver Injury.

This study aimed to compare the protective effects of different selenium supplements against heat stress and exercise fatigue-induced liver injury and to investigate the potential mechanisms of action. Selenium-enriched soybean protein (SePro), selenium-enriched soybean peptides (SePPs), and selenomethionine (SeMet) are organic selenium supplements in which selenium replaces the sulfur in their sulfur-containing amino acids. Common peptides (PPs) are obtained by enzymatic hydrolysis of soybean protein which was extracted from common soybean. The SePPs with higher hydrolysis degree and selenium retention were isolated via alkaline solubilization and acid precipitation and the enzymatic hydrolysis of alkaline protease, neutral protease, and papain. The results showed that SePPs could significantly increase the antioxidant levels in rats, inhibit lipid peroxidation, and reduce liver enzyme levels in rat serum, while the histological findings indicated that the inflammatory cell infiltration in the liver tissue was reduced, and new cells appeared after treatment with SePPs. Moreover, SePPs could increase glutathione (GSH) and GSH peroxidase (GSH-Px) in the liver, as well as protect the liver by regulating the NF-κB/IκB pathway, prevent interleukin 1ß (IL-1ß), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) release in the liver. The SePPs displayed higher antioxidant and anti-inflammatory activity in vivo than SePro, SeMet, Sodium selenite (Na2SeO3), and PPs. Therefore, SePPs could be used as a priority selenium resource to develop heatstroke prevention products or nutritional supplements.

Antioxidant activity of SSeCAHK in HepG2 cells: a selenopeptide identified from selenium-enriched soybean protein hydrolysates.

This paper is aimed at purifying and identifying selenium (Se)-containing antioxidative peptides from Se-enriched soybean peptides (SSP). In this work, the SSP was separated into five fractions (F1 to F5). Fraction F4, displaying the highest antioxidative activity, was further separated, and sub-fractions F4-1 to F4-5 were selected for antioxidative activity evaluation using 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2-azino-bis-(3-ethylbenzo-thiazoline-6-sulphonic acid)diammonium salt (ABTS), and OH- radical scavenging assays. The Se-containing antioxidative peptides with sequence Ser-SeC-Ala-His-Lys (SSeCAHK) were identified in sub-fraction F4-1 and chemically synthesized. This Se-containing pentapeptide showed a preventive effect against hydrogen peroxide (H2O2)-induced oxidative stress in HepG2 cells. Pretreating the cells for 2 h with SSeCAHK (0.13-0.50 mg mL-1) induced strong intracellular, reactive oxygen species (ROS) scavenging activity while preventing a decrease in reduced glutathione (GSH) and an increase in malondialdehyde (MDA). Therefore, SSeCAHK treatment improved H2O2-induced oxidative stress in HepG2 cells, demonstrating the significant potential of SSeCAHK as a natural antioxidative functional material for dietary supplementation.

Effect of Balint training in gastroenterology intern nurse practitioners: A systematic review protocol.

BACKGROUND: This study aims to assess the effect of Balint training (BT) in gastroenterology intern nurse practitioners (GINP) systematically. METHODS: This study will search EMBASE, MEDLINE, PsycINFO, Web of Science, Cochrane Library, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, and China National Knowledge Infrastructure from inception to the September 30, 2019 with no language limitation. In addition, we will also search grey records, such as conference abstracts and dissertations. Study quality will be checked using Cochran risk of bias tool. Statistical analysis will be performed using RevMan 5.3 software. RESULTS: This study will systematically evaluate the effect of BT in GINP and will provide evidence to judge whether BT is effective for GINP clinically. CONCLUSION: The results of this study may provide helpful evidence of BT in GINP in the clinical training.

Efficacy of furosemide for treatment of liver cirrhosis: A systematic review protocol of randomized controlled trial.

BACKGROUND: Previous clinical studies have reported that furosemide can be used to treat liver cirrhosis (LC) effectively. However, no study systematically explored this issue. This systematic review aims to investigate the efficacy and safety of furosemide for treatment of LC. METHODS: This study will be conducted through searching the following literature sources from their inception to February 28, 2019 without any language limitations: PUBMED, EMBASE, PsycINFO, Web of Science, Scopus, OpenGrey, Cochrane Library, Cumulative Index to Nursing and Allied Health Literature, Allied and Complementary Medicine Database, and Chinese Biomedical Literature Database. In addition, reference lists of relevant reviews and websites of clinical trial registry will also be searched. Only randomized controlled trials of furosemide for treatment of LC will be included in this study. Two reviewers will independently select studies, collect data, and determine risk of bias. RevMan 5.3 software will be used to pool the data and to conduct meta-analysis if sufficient studies will be included with acceptable heterogeneity. RESULTS: This study will investigate the efficacy and safety of furosemide for LC by the assessment of primary and secondary outcomes. The primary outcome includes mortality rate. The secondary outcomes consist of response rate, overall survival, body weight, urinary volume, quality of life, as measured by any relevant scales, and adverse events. CONCLUSION: The results of this study may provide summarized evidence of furosemide for the treatment of LC. ETHICS AND DISSEMINATION: No individual patient data will be used in this study, thus no ethics approval is needed. The findings of this study will be published in peer-reviewed journals.

Low molecular weight heparin improves proteinuria in rats with L-NAME induced preeclampsia by decreasing the expression of nephrin, but not podocin.

OBJECTIVE: We investigated the relationship between proteinuria in L-NAME induced preeclampsia and the expression of nephrin and podocin, and the effect of low-molecular-weight-heparin (LMWH) on proteinuria in rats. METHODS: We detected nephrin and podocin expression of kidneys of pregnant rats after L-NAME and after LMWH intervening pregnant rats. RESULTS: Glomerular nephrin expression in L-NAME induced preeclampsia significantly decreased, but not podocin. Nephrin was relatively increased after LMWH intervention and this was accompanied by a decrease in proteinuria. CONCLUSION: We demonstrate that down-regulation of nephrin is involved in L-NAME induced proteinuria, and that LMWH reduces proteinuria by up-regulation of neprhin.