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Recently, the protective effect of exosomes on ischemia/reperfusion (I/R) injury has become a research hotspot. The purpose of this study was to explore the therapeutic potential of microglia-derived exosomes on cerebral I/R injury. BV2 cell-derived exosomes (BV2-Exo) were extracted and characterized. The cerebral I/R model was constructed in vivo and intervened by using exosomes loaded with miR-302a-3p. The oxygen and glucose deprivation (OGD) model was constructed in vitro to simulate cerebral I/R injury. The binding sites of miR-302a-3p to Keap1 were analyzed by bioinformatics prediction and confirmed by dual-luciferase reporter assay. A study of whether exosomal miR-302a-3p affected cerebral I/R injury via the Keap1/Nrf2 axis was carried out by overexpression of keap1 (oe-keap1). Experimental results in vivo showed exosomal miR-302a-3p significantly repaired the cognitive impairment and suppressed the cell death of hippocampal neurons induced by cerebral I/R injury. Besides, exosomal miR-302a-3p inhibited the expression of ferroptosis-related proteins NCOA4, PTGS2, and p53 in cerebral I/R-treated mice. Bioinformatics prediction and double-luciferase reporter assay showed that Keap1 was the direct downstream target of miR-302a-3p. Experiment results in vitro showed that oe-Keap1 reversed the therapeutic effect of exosomal miR-302a-3p on cerebral I/R injury via the Keap1/Nrf2 axis, promoting the high expression of NCOA4, PTGS2, and p53 and the increase of Fe2+, MDA and ROS levels. These results demonstrated that microglia-exosomal miR-302a-3p suppressed ferroptosis to alleviate cerebral I/R injury by inhibiting neuronal ferritinophagy via regulating the Keap1/Nrf2 axis.

Objective: Recently, the protective effect of exosomes on ischemia/reperfusion (I/R) injury has become a research hotspot. The purpose of this study was to explore the therapeutic potential of microglia-derived exosomes on cerebral I/R injury. Methods: BV2 cell-derived exosomes (BV2-Exo) were extracted and characterized. The cerebral I/R model was constructed in vivo and intervened by using exosomes loaded with miR-302a-3p. The oxygen and glucose deprivation (OGD) model was constructed in vitro to simulate cerebral I/R injury. The binding sites of miR-302a-3p to Keap1 were analyzed by bioinformatics prediction and confirmed by dual-luciferase reporter assay. A study of whether exosomal miR-302a-3p affected cerebral I/R injury via the Keap1/Nrf2 axis was carried out by overexpression of keap1 (oe-keap1). Results: Experimental results in vivo showed exosomal miR-302a-3p significantly repaired the cognitive impairment and suppressed the apoptosis of hippocampal neurons induced by cerebral I/R injury. Besides, exosomal miR-302a-3p inhibited the expression of ferroptosis-related proteins NCOA4, PTGS2, and p53 in cerebral I/R-treated mice. Bioinformatics prediction and double-luciferase reporter assay showed that Keap1 was the direct downstream target of miR-302a-3p. Experiment results in vitro showed that oe-Keap1 reversed the therapeutic effect of exosomal miR-302a-3p on cerebral I/R injury via the Keap1/Nrf2 axis, promoting the high expression of NCOA4, PTGS2, and p53 and the increase of Fe2+, MDA and ROS levels. Conclusion: The results demonstrated that microglia-exosomal miR-302a-3p suppressed ferroptosis to alleviate cerebral I/R injury by inhibiting neuronal ferritinophagy via regulating the Keap1/Nrf2 axis.

In recent years, peptide self-assembly proved to be an efficient strategy to create complex structures or functional materials with nanoscale precision. In this work, we designed and synthesized a novel glycopeptide molecule with a galactose moiety through peptide galactosylation. Then relying on peptide self-assembling strategies, we created a supramolecular hydrogel with multivalent galactose ligands on the surface of self-assembled nanofibers for molecular recognition and interactions. Because of multivalent galactose–LecA interactions, the self-assemblies of glycopeptide could target P. aeruginosa specifically, and acted as anti-virulence and antibacterial agents to inhibit biofilm formation and bacterial growth of P. aeruginosa. Moreover, in association with polymyxin B, a common antibiotic, the glycopeptide hydrogel exhibited a synergistic growth inhibition effect on biofilm colonization of P. aeruginosa.

Glioma is a common and aggressive primary malignant brain tumor. MicroRNAs (miRNAs) play key roles in the post-transcriptional regulation of gene expression. Currently, miRNAs are considered to be useful biomarkers for the diagnosis and prognosis of glioma. Previously, we screened three differentially expressed miRNAs from Gene Expression Omnibus (GEO) database which included miRNA -338-3p. miRNA-338-3p is involved in tumor development in different cancers. However, in glioma, its function and its underlying mechanism remain unclear. We found that overexpression of miRNA -338-3p suppressed cell proliferation, migration, invasion, and promoted apoptosis of glioma in vitro. Myelin transcription factor 1-like (MYT1L) was found to be a direct target of miRNA-383-3p in glioma cells as the expression of MYT1L was inhibited by overexpressing miRNA-338-3p. Additionally, silencing MYT1L produced similar effects as overexpressing miRNA-338-3p in glioma cells. Overexpression of MYT1L also completely attenuated the inhibitory effect induced by miRNA-338-3p overexpression. These results suggest that the miRNA-338-3p/ MYT1L axis plays a critical role in the progression of glioma. Our study delineates one of the complex molecular mechanisms that drive the growth of glioma and may be useful in finding novel prognostic predictors and treatment targets in glioma. AVAILABILITY OF DATA AND MATERIALS: All data generated or analysed during this study are included in this published article.

In recent years, peptide self-assembly proved to be an efficient strategy to create complex structures or functional materials with nanoscale precision. In this work, we designed and synthesized a novel glycopeptide molecule with a galactose moiety through peptide galactosylation. Then relying on peptide self-assembling strategies, we created a supramolecular hydrogel with multivalent galactose ligands on the surface of self-assembled nanofibers for molecular recognition and interactions. Because of multivalent galactose-LecA interactions, the self-assemblies of glycopeptide could target

This paper puts forward the concept of exploration types and exploration models that can be used to find coal deposits. These were developed by taking into account the complexity and spatial differences of geological and geographical conditions of China's coalfield. ‘Exploration types’ here refers to groups of coal deposits similar in terms of the basic features of occurrence of the coal seams and the degree of difficulty of the exploration. ‘Exploration models’ here refers to generalizations and summations of advantageous geological conditions, effective technical exploration methods, and sound exploration programs and layout schemes suitable to different exploration types on the basis of the regularity of the occurrence of coal. Depending upon several factors that determine the degree of difficulty of exploration, such as regional geological conditions, the physical geographic environment, and the level of geological prospecting work performed, exploration for coal deposits can be divided into four types: (1) areas beneath and peripheral to old and existing coal mining zones in eastern China; (2) areas hidden by huge thick Cenozoic cover in eastern and central China; (3) geologically complex areas in eastern and southern China; and (4) geographically and geomorphologically complex areas in western China. In view of the different purposes and tasks involved in exploration, exploration models that are suited to different exploration types have been established, including the application of exploration methods, arrangement of exploration programs, and exploration engineering techniques. New exploration types and models promote the scientific and systematic features of coal geological exploratory engineering.