Hypoxic injury to the brain is very intricate under the control of biochemical reactions induced by various factors and mechanisms. Long non-coding RNAs (lncRNAs) have already been revealed to affect pathological processes in the nervous system of different degrees. This research aimed to investigate the mechanisms implicated in hypoxic brain injury. β-Asarone mitigated the decrease of cell viability, superoxide dismutase activity, and mitochondrial membrane potential, as well as the increase of cell apoptosis, lactate dehydrogenase release, malondialdehyde content, and reactive oxidative species production by cobalt chloride. LncRNA ribonuclease P RNA component H1 (RPPH1) was discovered to be highly expressed in hypoxia-induced PC12 cells, and β-Asarone addition led to a decline in RPPH1 expression. RPPH1 overexpression reversed the effect of β-Asarone on hypoxia-induced injury in PC12 cells. Furthermore, we proved that RPPH1 could sponge miR-542-3p. Subsequently, death effector domain containing 2 (DEDD2) was proven as the downstream gene of RPPH1/miR-542-3p axis. Eventually, the whole regulation mechanism of RPPH1/miR-542-3p/DEDD2 axis was testified through rescue assays. The impacts of β-Asarone on hypoxia-induced PC12 cells could be countervailed by RPPH1 augment, which was also discovered to be neutralized in response to miR-542-3p overexpression or DEDD2 depletion. These findings offered a novel perspective for understanding neuroprotection.

BackgroundEmerging evidence shows that exosomes play a crucial role in the occurrence and development of diabetes and its complications. The molecules in exosomes can be regarded as important markers for the diagnosis of diseases. However, it is presently unclear the pathological association mechanism between exosomes and diabetes.ResultsIn this study, transcriptome data and lncRNA regulatory association data of human pancreatic islet-derived exosome were integrated to construct the ceRNA network. Network analysis revealed that lncRNA with differential expression were primarily involved in islet insulin secretion signaling pathways, including Hippo, TGF-beta, Wnt, FOXO, Neurotrophin and ErbB signaling pathway. Further, combined with miRNA mediated competitive regulation and differential expression analysis results, potential markers of diabetes were revealed and validated in independent datasets. Finally, we analyzed the mechanisms of diabetes based on the competitive regulatory association and function of lncRNA.ConclusionOur results suggest that lncRNA such as lncRNA PVT1, LINC00960 and hsa-miR-107 might be involved in inflammation response in T1DM, and the former lncRNA chose in the present study may serve as novel biomarkers and potential targets for the diagnosis and treatment of T1DM.