MiR-107 Aggravates Oxygen-Glucose Deprivation/Reoxygenation (OGD/R)-Induced Injury Through Inactivating PI3K-AKT Signalling Pathway by Targeting FGF9/FGF12 in PC12 Cells.

OBJECTIVES: The aberrant expression of miR-107 has been confirmed in some neurological diseases, including ischemic stroke (IS). However, the function of miR-107 and underlying mechanisms are ambiguous. MATERIALS AND METHODS: Oxygen-Glucose Deprivation/Reoxygenation (OGD/R)-induced PC12 cells were used to mimic IS condition. MiR-107 expression and differentially expressed genes (DEGs) responding to IS were analyzed by GSE97532 and GSE61616 datasets, respectively. The target genes of miR-107 were predicted by TargetScan and confirmed by dual-luciferase reporter assay. Cell counting kit-8 and apoptosis assays were conducted to explore the role of miR-107 in biological behaviors of OGD/R-induced PC12 cells. RESULTS: Bioinformatics analysis revealed that miR-107 expression was elevated in rats with middle cerebral artery occlusion (MCAO), which was confirmed in OGD/R-treated PC12 cells. Notably, miR-107 strongly inhibited the proliferation of OGD/R-treated PC12 cells. As most DEGs were enriched in PI3K-AKT signaling pathway, which was critical for IS, DEGs in this pathway was compared with the down-regulated genes and the predicted genes to obtain potential target genes of miR-107, and ultimately fibroblast growth factor (FGF)9 and FGF12 stood out. The experiments demonstrated that miR-107 inhibited viability and promoted apoptosis of OGD/R-treated PC12 cells by down-regulating FGF9/FGF12 level. Mechanically, for the first time, we clarified the mechanism via which miR-107 inactivated PI3K-AKT signaling pathway by targeting FGF9/FGF12. CONCLUSIONS: We summarized that miR-107 aggravates OGD/R-induced injury through inactivating PI3K-AKT signaling pathway via targeting FGF9/FGF12. Therefore, our study elucidates the neurotoxicity of miR-107 in IS development and provides a new promising therapy strategy for IS.

Effects of gastrodin on 5-HT and neurotrophic factor in the treatment of patients with post-stroke depression.

Effects of gastrodin on 5-HT and neurotrophic factor in the treatment of patients with post-stroke depression (PSD) were investigated. A total of 78 PSD patients were selected in Binzhou City Center Hospital from September 2013 to December 2016. Patients were randomly divided into the control group and experimental group, 39 patients in each group. Patients in the control group were treated with conventional drug fluoxertine hydrochloride for 2 months, and patients in the experimental group were treated with gastrodin. The levels of 5-HT and neurotrophic factors in blood were measured using the enzyme-linked immunosorbent assay (ELISA) kit before, and at 1 and 2 months after treatment. The Hamilton Depression Scale (HAMD), Activities of Daily Living (ADL) scale, NIH Stroke Scale/Score (NIHSS) and Stroke Impact Scale (SIS) were used to evaluate the efficacy of treatment. Treatment efficacy was compared between the two groups. The levels of 5-HT and neurotrophic factors were significantly higher in the experimental group than those in the control group at 1 and 2 months after treatment (P<0.05), and HAMD, ADL, NIHSS and SIS scores were all better in the experimental group than in the control group (P<0.05). In addition, significantly less side effects were found in the experimental group than that in the control group, and treatment efficacy in the experimental group was significantly better than that in the control group (P<0.05). Gastrodin is effective in the treatment of PSD and should be popularized.