Injectable polylysine and dextran hydrogels with robust antibacterial and ROS-scavenging activity for wound healing.

Cutaneous wound management remains a major concern due to uncontrolled inflammation and bacterial infection in clinical care. A desirable hydrogel dressing with antibacterial and antioxidative properties can drive wound healing by inhibiting infection and inflammation. Herein, a multifunctional hydrogel based on polylysine-graft-cysteine (EPL-SH)/oxidized dextran (ODex) was fabricated for promoting skin tissue regeneration. The engineered hydrogel possessed versatile properties including tunable gelation time (60-300 s), typical rheological behavior, suitable swelling and degradation progress, injectable and self-healing ability. The unique hydrogels also displayed promising tissue adhesiveness, high cell affinity, excellent antioxidant and antimicrobial activity. Furthermore, the in vivo full-thickness skin defect experiment demonstrated the simple-to-implement injectable hydrogels could significantly promoting wound healing by improving the collagen deposition and angiogenesis. The manufacture of our multifunctional hydrogels dressing affords a new strategy for improving efficacy of cutaneous wound treatment.

Changes in structures and digestibility of amylose-oleic acid complexes following microwave heat-moisture treatment.

Amylose-oleic acid complexes (AOA) were exposed to microwave heat-moisture treatment (M-HMT) with different moisture content (MC), and the variations in structures and digestibility were investigated. M-HMT caused the dissociation of helical structures and destruction of short-range molecular order of AOA. Meanwhile, the molecules of amylose and oleic acid rearranged and more amylose-oleic acid complexes were formed during M-HMT, the complexing index of AOA was increased from 25.41 % to 41.20 % when treating at 35 % MC. Moreover, the relative content of single helix increased with increasing MC, resulting in higher V-type relative crystallinity. With ≥30 % MC, the treated complexes showed greater thermostability than that of original AOA. The treatment increased the enzymatic digestibility of AOA, and sample treated with 35 % MC had the highest resistant starch content of 82.33 %, which was 17.96 % higher than that of native AOA. The improved enzyme resistance should be correlated to increased molecular interplay and formation of amylose-oleic acid complexes.

High expression of ghrelin and obestatin prepropeptide in tumor tissues predicted adverse overall survival in gastric carcinoma patients.

BACKGROUND: Gastric cancer (GC) is the most prevailing digestive tract malignant tumor worldwide with high mortality and recurrence rates. However, its potential molecular mechanism and prognostic biomarkers are still not fully understood. We aim to screen novel prognostic biomarkers related to GC prognosis using comprehensive bioinformatic tools. METHODS: Four gene expression microarray data were downloaded from the Gene Expression Omnibus (GEO) database (GSE26942, GSE33335, GSE63089, and GSE79973). Differentially expressed genes (DEGs) between gastric carcinoma and normal gastric tissue samples were identified by an integrated bioinformatic analysis. Gene Ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed using statistical software R. STRING and Cytoscape software were employed to construct protein-protein interaction (PPI) networks. Hub genes with a high score of connectivity identified from the PPI network were identified. Prognostic values of hub genes were evaluated in GSE15459 dataset. Hub genes related to GC overall survival were further validated in GEPIA (Gene Expression Profiling Interactive Analysis) online tool. RESULTS: A total of 12 upregulated DEGs and 59 downregulated DEGs were identified when the 4 microarray data overlapped. Among them, 10 hub genes with a high score of connectivity were identified. High expression of ghrelin and obestatin prepropeptide (GHRL), BGN, TIMP metallopeptidase inhibitor 1, thrombospondin 2, secreted phosphoprotein 1, and low expression of CHGA were associated with a poor overall survival of gastric cancer (all log rank P < .05). After validation in GEPIA database, only GHRL was confirmed associated with a poor overall survival of gastric cancer (log rank P = .04). CONCLUSIONS: GHRL could be used as a novel biomarker for the prediction of a poor overall survival of gastric cancer, and could be a novel therapeutic target for gastric cancer treatment. However, future experimental studies are still required to validate these findings.

Long Noncoding RNA LINC01116 Contributes to Gefitinib Resistance in Non-small Cell Lung Cancer through Regulating IFI44.

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib, have been established as first-line treatments for non-small cell lung cancer (NSCLC) patients and have exhibited notable clinical efficacy. However, resistance to TKIs has become one of the major obstacles in improving the therapeutic efficacy of patients with NSCLC. This study aims to investigate the role of the long non-coding RNA (lncRNA) LINC01116 in gefitinib resistance of NSCLC and explore its underlying mechanism. In this study, we found that LINC01116 is upregulated in the gefitinib-resistant NSCLC cells and tissues. Loss- and gain-of-function assays uncovered that LINC01116 downregulation sensitized gefitinib resistance, whereas the overexpression of LINC01116 conferred PC9/R cells to gefitinib resistance. Moreover, LINC01116 silencing increased IFI44 expression. Overexpression of IFI44 reversed the resistance to gefitinib in PC9/R cells, and rescue experiments confirmed that LINC01116 affects the gefitinib resistance of PC9/R cells partly dependent on regulating IFI44 expression. Moreover, downregulation of LINC01116 increased the sensitivity of PC9/R cells to gefitinib in vivo. Our study demonstrates that LINC01116 plays a critical role in gefitinib resistance of NSCLC cells by affecting IFI44 expression, providing a novel therapeutic target to overcome TKI resistance in NSCLC.

Paeoniflorin on Rat Myocardial Ischemia Reperfusion Injury of Protection and Mechanism Research.

OBJECTIVE: To study the myocardial benefit effect and mechanism of paeoniflorin on myocardial ischemia reperfusion injury (MIRI) in rats. METHODS: Hundred SD rats were randomly divided into 5 groups: sham group, model group, Paeoniflorin (15 mg/kg) group, Paeoniflorin (30 mg/kg) group, and Paeoniflorin (60 mg/kg) group. Myocardial ischemia reperfusion model was established in each group except the sham group. The myocardial infarction and morphological changes were measured by the TTC staining and HE staining respectively. Myocardial caspase-3 was detected by immunohistochemistry. In addition, the protein levels of Bcl-2 and Bax and the expression ratio of p-erk, p-jnk, and p-p38 were detected by Western blot. Myocardial superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were measured by the assay kit. RESULTS: Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can obviously alleviate myocardial infarction caused by MIRI (p < 0.05). HE staining showed that the myocardial morphology in the treatment group was obviously better than that in the model group. WB and immunohistochemistry showed that Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can significantly increase the reduced protein level of bcl-2 (p < 0.05) and reduce the increased protein level of caspase3, bax -p-erk, p-jnk, and p-p38 caused by MIRI (p < 0.05). The activity of SOD was increased and the level of MDA was decreased after Paeoniflorin treatment. CONCLUSION: Paeoniflorin preconditioning has a protective effect on MIRI in rats. Its mechanism is related to reducing oxidative stress and apoptosis by inhibiting the expression of apoptosis-related signaling pathway.