The protective effects of phosphoserine aminotransferase 1 (PSAT1) against hepatic ischemia-reperfusion injury.

Hepatic ischemia-reperfusion (I/R) injury is a severe clinical syndrome, causing a profound medical and socioeconomic burden worldwide. This study aimed to explore underlying biomarkers and treatment targets in the progression of hepatic I/R injury. We screened gene expression profiles of the hepatic I/R injury from the Gene Expression Omnibus (GEO) database, downloaded expression profiles data (GSE117066). Differentially expressed genes (DEGs) were identified through cluster of the PPI network, and enrichment pathways were conducted based on gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) database. The bioinformatics analysis was used to identify biomarkers that alleviate hepatic I/R injury. Finally, the effects of hub gene were investigated by in vitro and in vivo experiments. A total of 162 DEGs (76 up-regulated and 86 down-regulated genes) were extracted between sham and I/R, and 248 DEGs (118 up-regulated and 130 down-regulated genes) were extracted between I/R and ischemic postconditioning (IPO). The cluster of the PPI network and maximal clique centrality (MCC) method of the common DEGs were performed to identify the phosphoserine aminotransferase 1 (PSAT1) as the potential gene for hepatic I/R injury. Then, the H-E, TUNEL and PCNA staining were indicated that the hepatic injury score was highest in I/R 6 h. The expression level of apoptosis-related proteins was consistent with the pathological results. Both gain- and loss-of-function assays demonstrated that hepatic I/R injury was alleviated by PSAT1. PSAT1 may play crucial roles in hepatic I/R injury and thus serves as a hub biomarker for hepatic I/R injury prognosis and individual-based treatment.

Effect of mesalazine combined with probiotics on inflammation and immune function of patients with inflammatory bowel disease.

OBJECTIVE: To determine the effects of mesalazine combined with probiotics on inflammation and immune function of patients with inflammatory bowel disease (IBD). METHODS: In this retrospective study, a total of 116 patients with IBD treated in Renmin Hospital of Wuhan University from September 2018 to September 2021 were enrolled and divided into a control group (n=55, treated with mesalazine alone) and a research group (n=61, treated with mesalazine combined with probiotics) according to the treatment regimen. The two groups were compared in the levels of inflammatory factors, immune factors, adverse reactions, clinical efficacy and improvement of patients' disease condition before and after treatment. Logistic regression was used to analyze the independent risk factors of infection in patients with IBD at 6 months after admission. RESULTS: The research group showed a significantly higher the total effective rate than the control group (P<0.05), and there was no notable difference between the two groups in the incidence of adverse reactions (P>0.05). In addition, compared with the control group, the research group showed significantly lower levels of immunoglobulin A (IgA), immunoglobulin G (IgG), immunoglobulin M (IgM), Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), and had significantly lower scores of clinical activity index (CAI) and endoscopic activity index (EAI) after treatment (all P<0.05). Higher IgG, IgM, IL-6, CRP and EAI levels at admission were independent risk factors for infection in patients with IBD. CONCLUSION: Mesalazine combined with probiotics can substantially improve the disease condition of patients with IBD, improve their immune ability and reduce their inflammation level, with a good safety profile.

The Role of Arachidonic Acid Metabolism in Myocardial Ischemia-Reperfusion Injury.

Patients with myocardial ischemic diseases or who are undergoing one of various heart treatments, such as open heart surgery, coronary artery bypass grafting, percutaneous coronary artery intervention or drug thrombolysis, face myocardial ischemia-reperfusion injury (MIRI). However, no effective treatment is currently available for MIRI. To improve the prognosis of people with cardiovascular disease, it is important to research the mechanism of MIRI. Arachidonic acid (AA) is one of the focuses of current research. The various metabolic pathways of AA are closely related to the development of cardiovascular disease, and the roles of various metabolites in ischemia-reperfusion injury have gradually been confirmed. AA is mainly metabolized in the cyclooxygenase (COX) pathway, lipoxygenase (LOX) pathway, and cytochrome P450 monooxygenase (CYP) pathway. This paper summarizes the progress of research on these three major AA metabolic pathways with respect to MIRI.

Effect of miRNA-19a on gastrointestinal motility in rats with functional dyspepsia.

The effect of microRNA (miRNA)-19a on gastrointestinal motility in rats with functional dyspepsia was investigated. Fifty adult Sprague-Dawley (SD) rats were randomly divided into 5 groups, 10 rats in each group, one group as the normal group, one group as the model group, and the other three groups were divided into negative control group, miRNA-19a mimic group and miRNA-19a inhibitor group. All rats were intraperitoneally injected with miRNA-19a scramble, miRNA-19a mimic and miRNA-19a inhibitor. Except the normal group, the functional dyspepsia model rat was established by proper clipping tail stimulation. The gastric emptying rate, intestinal propulsive ratio, serum motilin and vasoactive intestinal peptide of rats in each group were measured. The level of miRNA-19a expression in each group was detected by reverse transcription-polymerase chain reaction (RT-PCR). The gastric emptying rate, intestinal propulsive ratio and serum motilin in model group were significantly lower than those in normal group, and vasoactive intestinal peptide was higher in model group than that in normal group (P<0.05). The expression of miRNA-19a in model group was significantly higher than that in normal group (P<0.05). After intraperitoneal injection of miRNA-19a mimic, the expression of miRNA-19a was increased; gastric emptying rate, intestinal propulsive ratio and serum motilin were significantly reduced in model group, and vasoactive intestinal peptide was increased (P<0.05). After intraperitoneal injection of miRNA-19a inhibitor, the expression of miRNA-19a was remarkably decreased; gastric emptying rate, intestinal propulsive ratio and serum motilin were further increased in model group, and vasoactive intestinal peptide was decreased (P<0.05). In conclusion, the expression of miRNA-19a in rats with functional dyspepsia is higher than that in normal rats, and the reduced miRNA-19a expression can ameliorate the gastrointestinal motility in rats with functional dyspepsia.

NOR1 expression and its relationship with prognosis in patients with hepatocellular carcinoma.

PURPOSE: This study aimed to investigate the expression of NOR1 in hepatocellular carcinoma (HCC) tissue and its relationship with prognosis. METHODS: A sample of 60 specimens including HCC and adjacent normal tissues were collected from postoperative HCC patients from February to September 2011. Immunohistochemistry was used to detect the positive expression of the oxidored-nitro domain containing protein 1 (NOR1), the postoperative disease-free survival (DFS) rate and then the overall survival (OS) was analyzed by the Kaplan-Meier method. RESULTS: The results showed significantly lower expression of NOR1 in HCC tissue than that in adjacent normal tissue. Moreover, the OS and DFS rate of NOR1 (++) patients were significantly higher than those of other groups. CONCLUSION: Consequently, NOR1 is a protective protein in HCC, and the increase of its expression is favorable for the prognosis of patients.

Effects of selenium on myocardial apoptosis by modifying the activity of mitochondrial STAT3 and regulating potassium channel expression.

The present study investigated the effects of myocardial mitochondrial signal transduction and activator of transcription 3 (STAT3), succinate dehydrogenase activity and changes of potassium channel expression on cardiomyocyte apoptosis under low selenium conditions. Primary cultured cardiomyocytes from neonatal mice were divided into the non-toxic control group (0.1 µM sodium selenite) and low selenium treatment group (0.05 µM sodium selenite) according to different selenium concentrations. The expression of mitochondrial STAT3, p-STAT3, p-Kv1.2 potassium channel and apoptosis-related proteins, Bax and Bcl-2, were assessed by immunoblotting. Succinate dehydrogenase activity was measured by spectrophotometry. Flow cytometry was used to detect cardiomyocyte apoptosis. Low selenium treatment reduced the expression of p-STAT3, but did not affect the expression of STAT3. In addition, low selenium treatment reduced the activity of mitochondrial STAT3 and succinate dehydrogenase in cardiomyocytes, leading to injury of myocardial mitochondria. Compared with the control group, low selenium conditions reduced the activity of p-Kv1.2 and reduced the normal electrophysiological function of cardiomyocytes. In the low selenium-treated group, the expression of Bax protein increased, whereas the expression of Bcl-2 protein decreased. The apoptotic rate increased. In conclusion, selenium deficiency in cardiomyocytes leads to decreased potassium channel expression and decreased mitochondrial STAT3 activity and mitochondrial function, which in turn promotes the apoptosis of cardiomyocytes.