Magnolol supplementation alleviates diquat-induced oxidative stress via PI3K-Akt in broiler chickens.

This experiment was conducted to investigate the effects of magnolol on the oxidative parameters and jejunum injury induced by diquat in broiler chickens. This test adopts a 2 × 2 factors design, a total of 288 one-day-old male AA broiler chicks randomly allocated to four groups, consisting of six replicates of 12 birds each, which was then denoted as CON group, diquat (DIQ) group (16 mg/kg BW diquat was injected into birds at the age of 21 days), magnolol (MAG) group (basic bird diet supplemented with 300 mg/kg magnolol), and MAG + DIQ group. At 21 days of age, broilers in the DIQ group and the MAG + DIQ group were intraperitoneally injected with 16 mg/kg BW diquat. Results showed that diet supplementing with MAG could alleviate the decrease of ADG to a certain extent after exposure to DIQ. Addition of magnolol to the diet alleviated the decrease of ADG during injection, antioxidant enzymes, and gene expression and increased the markers of oxidative damage induced by diquat induction. Magnolol supplement reversed the increase of apoptotic cells in the diquat-induced chicken jejunum. RNA sequencing showed that PI3K-Akt, calcium, and NF-kappa B signaling pathways were the main enrichment pathways between the DIQ group and the MAG + DIQ group. Our findings revealed that magnolol may improve antioxidant enzyme activity and expression of related genes through the PI3K-Akt pathway to alleviate oxidative stress.

Expression and mechanism of long non-coding RNA HCG22 in oral squamous cell carcinoma / 华西口腔医学杂志

OBJECTIVES@#To investigate the expression and mechanism of the long non-coding RNA (lncRNA) HCG22 in oral squamous cell carcinoma (OSCC).@*METHODS@#HCG22 levels were detected in the OSCC and adjacent tissues, OSCC cells, and normal oral keratinocytes. HCG22 expression in SCC-25 and HSC-3 cells was upregulated by transfection of the overexpressing plasmi dvector. Methyl thiazolyl tetrazolium (MTT) assay, flow cytometry, and Transwell assay were employed to detect changes in cell proliferation, apoptosis, migration, and invasion ability, while Western blotting was used to detect the expression of epithelial-mesenchymal transformation-related proteins. The expression level of miR-650 in the cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR), and dual-luciferase reporter gene assay was applied to assess the targeting relationship between HCG22 and miR-650.@*RESULTS@#Compared with that in adjacent tissues, the expression of HCG22 significantly decreased in OSCC tissues (@*CONCLUSIONS@#HCG22 is expressed at low levels in OSCC. Upregulation of the expression of this lncRNA can inhibit the proliferation, migration, invasion, and epithelial-mesenchymal transition of OSCC cells. The mechanism of action of HCG22 may be related to its targeted regulation of miR-650.

Screening of biomarkers related with leukocyte responses early after burn injury in mice by differential gene expression profiling / 南方医科大学学报

<p><b>OBJECTIVE</b>To screen the genes related with leukocyte responses in mice early after burn injury by bioinformatic analysis of the gene expression profiling data.</p><p><b>METHODS</b>The gene expression profiles were obtained from GEO (GSE7404, Mouse musculus, 25% TBSA, full-thickness) database. T test, fold changes and GO functional enrichment analysis were used to identify the differentially expressed genes (DEGs) related to leukocyte responses to burns; the interacting genes were transferred to STRING to construct the protein-protein interaction (PPI) network. Biological annotation of the sub-networks was executed using the software Cytoscape. Real-time PCR and Western blotting were used to verify the DEGs in mice.</p><p><b>RESULTS</b>In mice at 1 day post-burn, a total of 658 genes were up-regulated and 1167 were down-regulated. PPI network and module analysis suggested that some of the genes (Stat1, Cdk1, Cd19, Lck and Jun) may play critical roles in the PPI network post-burn. Real-time PCR and Western blotting results in mice were consistent with those of bioinformatic analysis of Stat1, Cdk1 and Jun.</p><p><b>CONCLUSION</b>Stat1, Cdk1 and Jun might be critical players in the development of leukocyte response in mice early after burn injury. Our finding provides new insights into the pathogenesis of leukocyte response to burn injury and identifies several biomarkers as potential targets for burn treatment.</p>