No abstract

To investigate the function of miR‐454 in ischemic stroke, this study was carried out. Cerebral ischemia/reperfusion (I/R) injury animal model and a SHSY5Y cell culture model of oxygen‐glucose deprivation/reoxygenation (OGD/R) were constructed. The effects of miR‐454 were detected by evaluating the levels of biochemical markers, gene expression, and pathophysiological markers. The results showed that NOX4 level was elevated, while miR‐454 expression was reduced in I/R brain samples and in OGD/R‐treated cells. The miR‐454 agomir declined NOX4 level and reactive oxygen species (ROS) production in rats suffering from I/R. Furthermore, microRNA‐145 (miR‐454) overexpression inhibited NOX4 level and ROS production in cells treated by OGD/R and decreased luciferase activity in cells transfected with NOX4‐wild type (WT) reporter plasmid. Meanwhile, our results proved that the protected effects of miR‐454 on SH‐SY5Y cells treated by OGD/R were reversed by pcDNA‐NOX4 transfection. MiR‐454 protected animals from brain injury induced by cerebral I/R via directly regulating its target gene NOX4, illustrating a curatively potential target for treating ischemic stroke.

Granulocyte colony-stimulating factor (G-CSF) can effectively improve body’s immunity. This study explored G-CSF’s role in dopaminergic neurons apoptosis in Parkinson’s disease mice model. In this study, Oxidopamine, also known as 6-hydroxydopamine (6-OHDA) drugs were used to establish mouse models, and 2,3,5-Triphenyltetrazolium chloride (TTC) measurement of brain nerve cell apoptosis and mouse motor function scores methods were used to analyze and clarify whether G-CSF’s role in inflammatory process is through regulating monocyte chemoattractant protein 1 (MCP-1) expression and T cell immune function. Meanwhile, neutrophil infiltration in apoptotic and surrounding areas was also assessed. Nerve cell apoptosis was significantly reduced After a single dose of G-CSF treatment in the model 24 h after successful modeling, compared with PBS control group (P <0.05). The motor function of mice in the G-CSF treatment group was significantly improved (P <0.05) on days 7 and 14. Moreover, the expressions of MCP-1, IL-10, TNF-α, and TGF-β were significantly decreased through therapeutic intervention, and inflammation was controlled (P < 0.05). The number of CD11b infiltration in the apoptotic area in the G-CSF group did not increase, suggesting that intervention did not reduce apoptosis of nerve cells. Bcl-2 expression in the treatment group was significantly higher than in the control group, and Bax expression was lower (P <0.05). In addition, the number of dopamine BrdU+ cells in the substantia nigra was significantly increased (P <0.05). G-CSF can thus promote bone marrow hematopoiesis, thereby stimulating endogenous nerve cell proliferation, resisting nerve damage in Parkinson’s mice, and promoting neuron regeneration to help preserve neuronal function in mice and improve prognosis.