High­oxygen-modified atmospheric packaging delays flavor and quality deterioration in fresh-cut broccoli.

The purpose of this study was to investigate the impact of high­oxygen-modified atmospheric packaging (HOMAP) on aroma changes in fresh-cut broccoli during storage and to explore its regulatory mechanisms. The results showed that HOMAP reduced the levels of undesirable aroma substances hexanoic acid, isobutyric acid, cyclopentanone and increased glucosinolate accumulation by inhibiting the expression of arogenate/prephenate dehydratase (ADT), bifunctional aspartate aminotransferase and glutamate/aspartate-prephenate aminotransferase (PAT), thiosulfate/3-mercaptopyruvate Transferase (TST) to reduce the odor of fresh-cut broccoli. HOMAP inhibited the expression of respiratory metabolism related genes 6-phosphate fructokinase 1 (PFK), pyruvate kinase (PK), and NADH-ubiquinone oxidoreductase chain 6 (ND6). In HOMAP group, the low expression of phospholipase C (PLC), phospholipase A1 (PLA1), linoleate 9S-lipoxygenase 1 (LOX1) related to lipid metabolism and the high expression of naringenin 3-dioxygenase (F3H), trans-4-Hydroxycinnamate (C4H), glutaredoxin 3 (GRX3), and thioredoxin 1 (TrX1) in the antioxidant system maintained membrane stability while reducing the occurrence of membrane lipid peroxidation.

Multiomics analyses of the effects of LED white light on the ripening of apricot fruits.

INTRODUCTION: Apricot (Prunus armeniaca L.) fruits are highly perishable and prone to quality deterioration during storage and transportation. OBJECTIVES: To investigate the effects of LED white light treatment on postharvest ripening of fruits using metabolomics, transcriptomics, and ATAC-Seq analysis. METHODS: Fruits were exposed to 5 µmol m-2 s-1 LED white light for 12 h followed by 12 h of darkness at 20 °C daily for 12 days. The effects of the treatments on the physiological and nutritional quality of the fruits were evaluated. These data were combined with transcriptomic, metabolomic, and ATAC-Seq data from fruits taken on 8 d of treatment to provide insight into the potential mechanism by which LED treatment delays ripening. RESULTS: LED treatment activated pathways involved in ascorbate and aldarate metabolism and flavonoid and phenylpropanoid biosynthesis. Specifically, LED treatment increased the expression of UDP-sugar pyrophosphorylase (USP), L-ascorbate peroxidase (AO), dihydroflavonol 4-reductase (DFR), chalcone synthase (CHS), and caffeoyl-CoA O-methyltransferase (CCOAOMT1), leading to the accumulation of caffeoyl quinic acid, epigallocatechin, and dihydroquercetin and the activation of anthocyanin biosynthesis. LED treatment also affected the expression of genes associated with plant hormone signal transduction, fruit texture and color transformation, and antioxidant activity. The notable genes affected by LED treatment included 1-aminocyclopropane-1-carboxylate synthase (ACS), 1-aminocyclopropane-1-carboxylate oxidase (ACO), hexokinase (HK), lipoxygenase (LOX), malate dehydrogenase (MDH), endoglucanase (CEL), various transcription factors (TCP, MYB, EFR), and peroxidase (POD). ATAC-Seq analysis further revealed that LED treatment primarily regulated phenylpropanoid biosynthesis. CONCLUSION: The results obtained in this study provide insights into the effects of LED light exposure on apricot fruits ripening. LEDs offer a promising approach for extending the shelf life of other fruits and vegetables.

Extracellular matrix physical properties govern the diffusion of nanoparticles in tumor microenvironment.

Nanoparticles (NPs) are confronted with limited and disappointing delivery efficiency in tumors clinically. The tumor extracellular matrix (ECM), whose physical traits have recently been recognized as new hallmarks of cancer, forms a main steric obstacle for NP diffusion, yet the role of tumor ECM physical traits in NP diffusion remains largely unexplored. Here, we characterized the physical properties of clinical gastric tumor samples and observed limited distribution of NPs in decellularized tumor tissues. We also performed molecular dynamics simulations and in vitro hydrogel experiments through single-particle tracking to investigate the diffusion mechanism of NPs and understand the influence of tumor ECM physical properties on NP diffusion both individually and collectively. Furthermore, we developed an estimation matrix model with evaluation scores of NP diffusion efficiency through comprehensive analyses of the data. Thus, beyond finding that loose and soft ECM with aligned structure contribute to efficient diffusion, we now have a systemic model to predict NP diffusion efficiency based on ECM physical traits and provide critical guidance for personalized tumor diagnosis and treatment.

Immunotherapy discovery on tumor organoid-on-a-chip platforms that recapitulate the tumor microenvironment.

Cancer immunotherapy has achieved remarkable success over the past decade by modulating patients' own immune systems and unleashing pre-existing immunity. However, only a minority of cancer patients across different cancer types are able to benefit from immunotherapy treatment; moreover, among those small portions of patients with response, intrinsic and acquired resistance remains a persistent challenge. Because the tumor microenvironment (TME) is well recognized to play a critical role in tumor initiation, progression, metastasis, and the suppression of the immune system and responses to immunotherapy, understanding the interactions between the TME and the immune system is a pivotal step in developing novel and efficient cancer immunotherapies. With unique features such as low reagent consumption, dynamic and precise fluid control, versatile structures and function designs, and 3D cell co-culture, microfluidic tumor organoid-on-a-chip platforms that recapitulate key factors of the TME and the immune contexture have emerged as innovative reliable tools to investigate how tumors regulate their TME to counteract antitumor immunity and the mechanism of tumor resistance to immunotherapy. In this comprehensive review, we focus on recent advances in tumor organoid-on-a-chip platforms for studying the interaction between the TME and the immune system. We first review different factors of the TME that recent microfluidic in vitro systems reproduce to generate advanced tools to imitate the crosstalk between the TME and the immune system. Then, we discuss their applications in the assessment of different immunotherapies' efficacy using tumor organoid-on-a-chip platforms. Finally, we present an overview and the outlook of engineered microfluidic platforms in investigating the interactions between cancer and immune systems, and the adoption of patient-on-a-chip models in clinical applications toward personalized immunotherapy.

Infliximab is effective in the treatment of ulcerative colitis with dermatomyositis: A case report.

BACKGROUND: Joint, skin, oral cavity, and eye lesions are the most common extraintestinal manifestations of ulcerative colitis that can occur before or after its onset. The cases of ulcerative colitis with dermatomyositis (DM) are rare. In this study, we report a rare case of ulcerative colitis with DM that was effectively treated with infliximab. CASE SUMMARY: The patient was a 57-year-old female with a 2-year history of DM. The patient was admitted to hospital with abdominal pain, diarrhea, and blood in stool lasting for more than 2 mo. Colonoscopy revealed multiple erosions and ulcers in the entire colon and rectum. Pathological sections showed chronic inflammatory cell infiltration, especially neutrophil infiltration, in the colonic mucosa; therefore, the patient was diagnosed with ulcerative colitis. Preparations of 5-aminosalicylic acid was added to her treatment based on the original treatment for DM, but its effect was unsatisfactory. The patient's discomfort was relieved after infliximab treatment. CONCLUSION: Infliximab can improve DM in the treatment of ulcerative colitis. Specialists need to raise awareness about patients with inflammatory bowel disease who have rare extraintestinal manifestations.

Effect of three-dimensional ECM stiffness on cancer cell migration through regulating cell volume homeostasis.

The extracellular matrix (ECM) stiffness has direct effect on cancer cells homeostasis (e.g., cell volume), which is critical for regulation of their migration. However, the relationship among ECM stiffness, cell volume and cancer cell migration in three-dimensional (3D) microenvironment remains elusive. In this work, we prepared the collagen-alginate hydrogels with tunable stiffness to study how the 3D ECM stiffness influences cell volume and their migration. We found the cell volume homeostasis and migration speed of the MDA-MB-231 cells are both regulated by 3D ECM stiffness, while cell migration speed shows the same stiffness-dependent trend with cell volume. Deviating the cell volume from its homeostasis state can cause a significant decrease in its migration ability, which can be recovered through recovering the cell volume to its homeostasis state. This work reveals for the first time that 3D ECM stiffness regulates cell migration behavior through regulating cell volume homeostasis, which may provide a novel view in the exploration of the underlying mechanisms of cancer metastasis and cellular mechanotransduction.

Oxycodone vs Sufentanil in Patient-Controlled Intravenous Analgesia After Gynecological Tumor Operation: A Randomized Double-Blind Clinical Trial.

BACKGROUND: This study aims to compare analgesic effect and side effects of oxycodone and sufentanil in transition analgesia and patient-controlled intravenous analgesia (PCIA) after gynecological tumor operation under general anesthesia. PATIENTS AND METHODS: A prospective, randomized, double-blind research was conducted. Patients undergoing elective gynecological tumor surgery were randomized into four groups: Group S (sufentanil transition analgesia and sufentanil PCIA), Group OS (oxycodone transition analgesia and sufentanil PCIA), Group SO (sufentanil transition analgesia and oxycodone PCIA) and Group O (oxycodone transition analgesia and oxycodone PCIA). The primary outcomes were Numerical Rating Scale (NRS) at rest and coughing, accumulated opioid consumption in PCIA and patients' satisfaction. RESULTS: Patients in Group OS and Group O showed shorter time of consciousness recovery and extubation after surgery. Accumulated opioid consumption in PCIA (equal to morphine) in Group SO and Group O was significantly less than that in Group S and Group OS. Patients in Group O showed lower NRS at rest and coughing, but higher patients' satisfaction 3, 24 and 48 hours after surgery. Patients in Group SO and Group O showed a shorter time of intestinal recovery, first feeding and first-time movement. CONCLUSION: Both oxycodone and sufentanil provided adequate pain relief in transitional analgesia and PCIA treatment after surgery. Oxycodone without background infusion showed less analgesic drug consumption and faster recovery than sufentanil with background infusion in PCIA after gynecological tumor operation under general anesthesia.

Cell mechanical microenvironment for cell volume regulation.

Cell volume regulation, as one of the fundamental homeostasis of the cell, is associated with many cellular behaviors and functions. With the increased studies on the effect of environmental mechanical cues on cell volume regulation, the relationship between cell volume regulation and mechanotransduction becomes more and more clear. In this paper, we review the mechanisms and hypotheses by which cell maintains its volume homeostasis both in vivo and in constructed cell mechanical microenvironment (CMM) in vitro. We discuss how the growth-division regulation maintains the volume homeostasis of cells in the cell cycle and how the cell cortex/membrane tension mediates the effect of CMM (i.e., osmotic pressure, matrix stiffness, and mechanical force) on cell volume regulation. We also highlight the roles of cell volume as a perfect integrator of the downstream signals of mechanotransduction from different aspects of CMM and an effective indicator for the mechanical condition that cell confronts. This interdisciplinary perspective can provide new insight into biomechanics and may shed light on bioengineering and pathological research work. We hope this review can facilitate future studies on the investigation of the role of cell volume in mechanotransduction.

Microchannel Stiffness and Confinement Jointly Induce the Mesenchymal-Amoeboid Transition of Cancer Cell Migration.

The physical confinement of cell microenvironment could enhance the invasive capability and drug resistance of cancer cells. However, due to the lack of in vitro experimental platform to mimic both stiffness and confinement of the tumor microenvironment, the underlying mechanism remains elusive. Here, we developed a hydrogel-based microchannel platform with independently tunable channel stiffness and width in a physiological range. We found that the migration speed of the cancer cell is influenced by the synergistic effect of channel stiffness and width. In addition, the mesenchymal-amoeboid transition has a strong correlation with the channel stiffness. Besides, with a developed computational model, the role of nuclear stiffness on cancer migration speed and thus the mesenchymal-amoeboid transition in microchannels was also revealed. This platform is capable of mimicking the native physical microenvironment during metastasis, providing a powerful tool for high-throughput screening applications and investigating the interaction between cancer migration and biophysical microenvironment.

Foxo3a-dependent miR-633 regulates chemotherapeutic sensitivity in gastric cancer by targeting Fas-associated death domain.

The development of chemotherapeutic drugs resistance such as doxorubicin (DOX) and cisplatin (DDP) is the major barrier in gastric cancer therapy. Emerging evidences reveal that microRNAs (miRNAs) contribute to chemosensitivity. In this study, we investigated the role of miR-633, an oncogenic miRNA, in gastric cancer chemoresistance. In gastric cancer tissue and cell lines, miR-633 expression was highly increased and correlated with down regulation of Fas-associated protein with death domain (FADD). Inhibition of miR-633 significantly increased FADD protein level and enhanced DOX/DDP induced apoptosis in vitro. MiR-633 antagomir administration remarkably decreased tumor growth in combination with DOX in vivo, suggesting that miR-633 targets FADD to block gastric cancer cell death. We found that the promoter region of miR-633 contained putative binding sites for forkhead box O 3 (Foxo3a), which can directly repress miR-633 transcription. In addition, we observed that DOX-induced nuclear accumulation of Foxo3a leaded to the suppression of miR-633 transcription. Together, our study revealed that miR-633/FADD axis played a significant role in the chemoresistance and Foxo3a regulated this pathway in gastric cancer. Thus, miR-633 antagomir resensitized gastric cancer cells to chemotherapy drug and had potentially therapeutic implication.

Oxycodone versus sufentanil in adult patient-controlled intravenous analgesia after abdominal surgery: A prospective, randomized, double-blinded, multiple-center clinical trial.

BACKGROUND: A randomized controlled trial was performed to compare analgesic effects and adverse effects of oxycodone and sufentanil in patient-controlled intravenous analgesia (PCIA) after abdominal surgery under general anesthesia. METHODS: Adult patients undergoing elective abdominal surgery were randomly allocated into oxycodone and sufentanil groups according to the randomization sequence. Study personnel, health-care team members, and patients were masked to the group assignment throughout the study period. Oxycodone (0.1 mg/kg for endoscopy; 0.15 mg/kg for laparotomy) or sufentanil (0.1 µg/kg for endoscopy; 0.15 µg/kg for laparotomy) was administrated at the end of surgeries. Postoperative pain was controlled using PCIA. Bolus dose was 2 mg and 2 µg for oxycodone and sufentanil group, respectively. The lockout time was 5 minutes for all patients, and there was no background infusion for oxycodone group, whereas 0.02 µg/kg/h background infusion was administrated in sufentanil group. The primary outcomes were the total analgesic doses in PCIA, effective bolus times, the length of first bolus since patients returning to ward from postanesthesia care unit (PACU), rescue analgesic rate in PACU, numeric rating scales, functional activity scores, and patients' satisfaction scores. RESULTS: A total of 200 patients were screened, and 175 patients were enrolled. Patients were randomly assigned to oxycodone (n = 87) and sufentanil (n = 88) groups. Both oxycodone and sufentanil PCIA provided adequate postoperative pain relief. Patients in oxycodone group showed a shorter consciousness recovery time after surgery. The major adverse effect in patients from oxycodone group was nausea/vomiting, whereas multiple adverse complications including nausea/vomiting, pruritus, and respiratory depression were observed in patients from sufentanil group. Patients from oxycodone group showed significantly reduced analgesic drug consumption (calculated as equivalent dose of morphine), functional activity scores, and patient satisfaction scores. DISCUSSION: Compared with sufentanil PCIA, oxycodone PCIA showed better analgesic effects, lower incidence of adverse complications, and less analgesic drug consumption during postoperative pain management.

MiR-9 is involved in TGF-ß1-induced lung cancer cell invasion and adhesion by targeting SOX7.

MicroRNA (miR)-9 plays different roles in different cancer types. Here, we investigated the role of miR-9 in non-small-cell lung cancer (NSCLC) cell invasion and adhesion in vitro and explored whether miR-9 was involved in transforming growth factor-beta 1 (TGF-ß1)-induced NSCLC cell invasion and adhesion by targeting SOX7. The expression of miR-9 and SOX7 in human NSCLC tissues and cell lines was examined by reverse transcription-quantitative polymerase chain reaction. Gain-of-function and loss-of-function experiments were performed on A549 and HCC827 cells to investigate the effect of miR-9 and SOX7 on NSCLC cell invasion and adhesion in the presence or absence of TGF-ß1. Transwell-Matrigel assay and cell adhesion assay were used to examine cell invasion and adhesion abilities. Luciferase reporter assay was performed to determine whether SOX7 was a direct target of miR-9. We found miR-9 was up-regulated and SOX7 was down-regulated in human NSCLC tissues and cell lines. Moreover, SOX7 expression was negatively correlated with miR-9 expression. miR-9 knockdown or SOX7 overexpression could suppress TGF-ß1-induced NSCLC cell invasion and adhesion. miR-9 directly targets the 3' untranslated region of SOX7, and SOX7 protein expression was down-regulated by miR-9. TGF-ß1 induced miR-9 expression in NSCLC cells. miR-9 up-regulation led to enhanced NSCLC cell invasion and adhesion; however, these effects could be attenuated by SOX7 overexpression. We concluded that miR-9 expression was negatively correlated with SOX7 expression in human NSCLC. miR-9 was up-regulated by TGF-ß1 and contributed to TGF-ß1-induced NSCLC cell invasion and adhesion by directly targeting SOX7.

Neuroprotective effects of sevoflurane against electromagnetic pulse-induced brain injury through inhibition of neuronal oxidative stress and apoptosis.

Electromagnetic pulse (EMP) causes central nervous system damage and neurobehavioral disorders, and sevoflurane protects the brain from ischemic injury. We investigated the effects of sevoflurane on EMP-induced brain injury. Rats were exposed to EMP and immediately treated with sevoflurane. The protective effects of sevoflurane were assessed by Nissl staining, Fluoro-Jade C staining and electron microscopy. The neurobehavioral effects were assessed using the open-field test and the Morris water maze. Finally, primary cerebral cortical neurons were exposed to EMP and incubated with different concentration of sevoflurane. The cellular viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assayed. TUNEL staining was performed, and the expression of apoptotic markers was determined. The cerebral cortexes of EMP-exposed rats presented neuronal abnormalities. Sevoflurane alleviated these effects, as well as the learning and memory deficits caused by EMP exposure. In vitro, cell viability was reduced and LDH release was increased after EMP exposure; treatment with sevoflurane ameliorated these effects. Additionally, sevoflurane increased SOD activity, decreased MDA levels and alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, Bax and Bcl-2. These findings demonstrate that Sevoflurane conferred neuroprotective effects against EMP radiation-induced brain damage by inhibiting neuronal oxidative stress and apoptosis.

The effect of sevoflurane inhalation on gabaergic neurons activation: observation on the GAD67-GFP knock-in mouse.

The mechanisms underlying volatile anesthesia agents are not well elucidated. Emerging researches have focused on the participation of γ-aminobutyric acid (GABA) neurons but there still lacks morphological evidence. To elucidate the possible activation of GABAergic neurons by sevoflurane inhalation in morphology, Fos (as neuronal activity marker) and GABA neurons double labeling were observed on the brain of glutamic acid decarboxylase (GAD) 67-GFP knock-in mice after sevoflurane inhalation. Twenty GAD67-GFP knock-in mice were divided into three groups: S1 group: incomplete anesthesia state induced by sevoflurane; S2 group: complete anesthesia state induced by sevoflurane; control(C) group. Sevoflurane induced a significant increase of Fos expression in the dorsomedial hypothalamic nucleus (DM), periaqueductal grey (PAG), hippocampus (CA1, DG), paraventricular thalamic nucleus (PV), lateral septal nucleus (LS), and cingulate cortex (Cg1 and Cg2) in S1 group compared to C group, and increase of Fos expression in S2 group compared to S1 group. In S2 group, Fos was only expressed in the medial amygdaloid nucleus (MeA), Edinger-Westphal (E-W) nucleus, arcuate hypothalamic nucleus (Arc) and the ventral part of paraventricular hypothalamic nucleus (PaV). Double immunofluroscent staining indicated that in LS, almost all Fos were present in GABAergic neurons. In CA1, DG, DM, cg1, cg2, and PAG, Fos was expressed as well, but only few were present in GABAergic neurons. Fos expression was very high in thalamus, but no coexistence were found as no GABAergic neuron was detected in this area. Our results provided morphological evidence that GABAergic transmission in specific brain areas may participate in the sevoflurane-induced anesthesia.

The effect of ketamine on N-methyl-D-aspartate receptor subunit expression in neonatal rats.

BACKGROUND AND OBJECTIVE: Ketamine has been widely used in paediatric anaesthesia but its influence on development in infants and toddlers still remains unclear. In order to elucidate the influence of ketamine on brain development in neonatal rats, semiquantitative reverse transcriptase PCR, quantitative reverse transcriptase PCR and immunohistochemistry assays were performed to detect the expression of N-methyl-D-aspartate receptor subtypes expression. METHODS: Seven-day-old rats were divided into two random groups. All of them were injected with ketamine intraperitoneally at postnatal day (PND) 7; one group was sacrificed at PND 7, but the other group was sacrificed at PND 28. Each group was divided into five random subgroups. RESULTS: In the semiquantitative reverse transcriptase PCR and quantitative reverse transcriptase PCR experiments, ketamine treatment caused a marked increase in mRNA expression in all subtypes at PND 7 and in NR2A subtypes at PND 28. Immunohistochemistry results indicated that NR2A, 2B and 2C receptor protein increased significantly at PND 7, and NR2A receptor protein increased at PND 28. CONCLUSIONS: Exposure to ketamine resulted in an increase in N-methyl-D-aspartate receptor subunits at PND 7, and this increase persisted to PND 28 in NR2A.

Hyperoxygenated solution preconditioning attenuates lung injury induced by intestinal ischemia reperfusion in rabbits.

BACKGROUND: The current study was undertaken to elucidate the possible therapeutic effects of hyperoxygenated solution (HOS) preconditioning on lung injury induced by intestinal ischemia/reperfusion (I/R) in rabbits. MATERIALS AND METHODS: Eighty rabbits were randomly divided into four groups (n = 20 each) as follows: (1) control group in which sham operation was performed (sham group), (2) HOS pretreatment group and sham operation (HOS + sham group), (3) ischemia/reperfusion group (I/R group), (4) HOS pretreatment and ischemia/reperfusion group (HOS + I/R group). Intestinal I/R model was produced by clamping superior mesenteric artery with an atraumatic vascular clamp for 1 h, and followed by reperfusion for 2 h. Animals in HOS + sham group and HOS + I/R group received intravenous HOS infusion (20 mL/kg, 10 mL/kg.h for 2 h) every day for 5 d before operation, and animals in sham group and I/R group received the same amount of normal saline in the same way. At the end of reperfusion, 8 animals from every group were sacrificed and histopathological changes of lung were observed; pulmonary edema, lung myeloperoxidase activity, superoxide dismutase activity, and malondialdehyde levels in lung tissues were also detected. The rest 12 animals in every group underwent 60 min of intestinal ischemia followed by 72 h of reperfusion, and effects of HOS pretreatment on survival in rabbits with lung injury induced by intestinal I/R was observed. RESULTS: When rabbits were subjected to 60 min of intestinal ischemia, a high incidence of mortality was observed within 24 h. In this situation, HOS preconditioning before the start of ischemia/reperfusion significantly reduced the mortality. HOS preconditioning also decreased lung wet/dry ratio, neutrophil infiltration, lipid membrane peroxidation, and increased superoxide dismutase activity in the lungs after intestinal I/R compared with the I/R-treated rabbit lungs without HOS treatment. Histopathological analysis also indicated the effectiveness of HOS pretreatment. CONCLUSIONS: HOS preconditioning could preserve superoxide dismutase activity, decrease lipid membrane peroxidation and neutrophil infiltration in the lungs, then ameliorate the deleterious changes in pulmonary injury induced by intestinal I/R.

Protective effects of hyperoxygenated solution preconditioning on intestinal ischemia-reperfusion injury in rabbits.

BACKGROUND: The aim of this study was to investigate the protective effects of hyperoxygenated solution (HOS) preconditioning on intestinal ischemia-reperfusion (IR) injury in rabbits. MATERIALS AND METHODS: Thirty-two rabbits were randomly divided into four groups as follows: (1) control group in which sham operation was performed (Sham group); (2) sham operation and HOS treatment group (sham+H group); (3) ischemia-reperfusion group (IR group); (4) ischemia-reperfusion and HOS treatment group (H group). Intestinal IR model was produced by clamping superior mesenteric artery with an atraumatic vascular clamp for 1 h, followed by reperfusion for 2 h. Animals in H group received intravenous HOS infusion (20 mL/kg) every day for 5 days before ischemia-reperfusion; animals in the sham+H group received the same amount of HOS before sham operation, and animals in IR group received the same amount of normal saline in the same way. At the end of reperfusion, histopathological changes of intestine were observed, and malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities in intestinal tissues were also detected. Intestinal barrier function was assessed by blood d-lactate levels and bacterial translocation (BT). RESULTS: The H group showed significantly lower MDA levels and higher activities of SOD, CAT, and GSH-Px in the intestinal tissue compared with the IR group. Furthermore, the mean d-lactate levels and incidence of BT in the H group were significantly lower than those in the IR group. Histopathological analysis also indicated that there were significant histological improvements in the H group compared with the IR group. CONCLUSIONS: HOS preconditioning at an appropriate dose ameliorates the deleterious changes in intestinal mucosal injury and barrier function associated with IR by effectively preventing a decrease in the intestinal antioxidant defense system, which is another simple and effective measure to protect intestine from IR injury.