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Objective To explore the effect of miR-433 on oxidative stress and cognitive function in the hippocampus of rats with postoperative cognitive impairment (POCD) and its mechanism of action. Methods Rats were randomly divided into 4 groups, control group, POCD group, POCD+NC mimic group, and POCD+miR-433 mimic group. A rat POCD model was constructed, and the expression of miR-433 in hippocampal tissue of POCD rats was detected by real-time fluorescence quantitative PCR assay (RT-qPCR). Morris Water Maze test was used to evaluate the cognitive function of rats. Hematoxylin and Eosin (HE) staining was used to detect histopathological changes in hippocampus. TUNEL staining was used to detect cell apoptosis. The level of oxidative stress was detected by enzyme-linked immunosorbent assay (ELISA). Dual luciferase reporter gene system was used to detect the targeting relationship between miR-433 and JAK2. Western blotting was used to detect the expression of cleaved caspase-3, Bad, Bcl-2, JAK2, p-JAK2, STAT3, and p-STAT3 proteins in the hippocampus tissues. Results Compared with the control group, miR-433 expression in hippocampus tissues of rats in the POCD group was significantly reduced. The evasion latency was prolonged. The number of crossing the target platform was reduced. Neuronal cells in the POCD group were disordered. The number of cells was significantly reduced. The apoptosis rate of neuronal cells was significantly increased. Cleaved caspase-3 and Bad protein expression was significantly increased. Bcl-2 protein expression and superoxide dismutase (SOD) level significantly decreased. Malondialdehyde (MDA) level increased significantly. The difference was statistically significant (P ＜ 0. 05). Compared with the POCD + NC mimic group, the expression of miR-433 in hippocampus tissues of rats in the POCD + miR-433mimic group was significantly higher, the escape latency was shortened, the number of crossing the target platform was increased, the arrangement of cells in the hippocampus was more regular. The apoptosis rate of neuronal cells was significantly lower, and the rate of neuronal cell apoptosis was significantly reduced. The expression of cleaved caspase-3 and Bad protein expression was significantly decreased. Bcl-2 protein expression was significantly increased, SOD level was significantly increased, and MDA level was significantly decreased. The results of dual luciferase reporter gene assay showed that JAK2 was the target gene of miRNA-433, and compared with POCD + miR-433 mimic + Vector group, the hippocampal tissues of rats in POCD + miR-433mimic + pcDNA-JAK2 group showed significantly lower expression of JAK2, p-JAK2, p-STAT3, cleaved caspase-3, Bad protein, and MDA levels were significantly increased, while Bcl-2 protein and SOD levels were significantly decreased. The difference was statistically significant (P ＜ 0. 05). Conclusion MiR-433 inhibits oxidative stress through JAK2/STAT3 signaling pathway to prevent postoperative cognitive impairment in rats. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of human antigen R (HuR) in glioma and its possible mechanism. Methods 21 cases of glioma tissue and normal control tissue were collected. Normal glioma cell line SVGp12 and human glioblastoma-derived cell line U251 were cultured in vitro, qRT-PCR was used to detect the mRNA expression of HuR and polypyrimidine tract-binding protein 1 (PTBP1) in tissues and cells. Western Blot was used to detect the protein expression of HuR, PTBP1, phosphorylated protein kinase B(p-Akt) and protein kinase B (Akt) in tissues and cells. RNA-binding protein immunoprecipitation test was used to detect the regulatory effect of HuR on PTBP1. CCK-8 was used to detect cell viability. EdU test was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. Results Compared with the normal control group, the mRNA and protein expression of HuR, and the mRNA and protein expression of PTBP1 in the glioma group were significantly increased (all P < 0. 05). Compared with the SVGp12 group, the mRNA and protein expression of HuR, and the mRNA and protein expression of PTBP1 in the U251 group were significantly increased (all P < 0. 05). HuR regulated the expression of PTBP1 by binding to PTBP1 mRNA. There was no statistically significant difference in the indicators between the blank group and the si-NC + oe-NC group (all P > 0. 05). Compared with the si-NC + oe-NC group, the mRNA and protein expressions of HuR and PTBP1 in the si-HuR group + oe-NC group were significantly reduced (all P < 0. 05), and the cell viability at 48 h and 72 h and the proliferation ability of cell were significantly reduced (all P < 0. 05), cell apoptosis was significantly increased (P < 0. 05), and the protein expression of p-Akt/Akt was significantly reduced (P < 0. 05). Compared with the si-HuR + oe-NC group, the mRNA and protein expression of HuR in the cells of the si-HuR + oe-PTBP1 group was not statistically different (all P > 0. 05), while the expression of PTBP1 mRNA and protein was significantly increased (all P < 0. 05), cell viability at 48 h and 72 h and the proliferation ability of cell were significantly increased (all P < 0. 05). Cell apoptosis was significantly reduced (P < 0. 05), and the protein expression of p-Akt/Akt was significantly increased (P < 0. 05). Conclusion HuR may activate Akt pathway by up-regulating the expression of PTBP1 to promote the proliferation of glioma cells and inhibit cell apoptosis. [ABSTRACT FROM AUTHOR]

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Object To explore the expressions and their significance of the hypoxia-inducible factor ( HIF )-1α and vascular endothelial growth factor (VEGF) in pituitary adenomas. Methods The mRNA expressions of HIF-1α and VEGF were determined by reverse transcription polymerase chain reaction (RT-PCR), and the protein expressions of HIF-1α and VEGF were measured by immunostaining in total 42 patients who were divided into invasive and non-invasive pituitary adenoma groups. The differences of HIF-1α and VEGF mRNA expression between different groups were compared by Pearson's correlation coefficient and the protein expression by Spearman's correlation coefficient. Results The protein expressions of HIF-1α and VEGF in invasive pituitary adenoma group were significant higher than those in non-nvasive pituitary adenoma group (χ2 =9.147, P<0.05 and χ2 =5.401, all P<0.05). There were significant difference of VEGF mRNA expression between invasive and non-invasive pituitary adenoma groups (P<0.05). The correlated analyses of mRNA and protein expression showed there was a negative relation between HIF-1α and VEGF in non-invasive pituitary adenoma groups (P >0.05), and a positive relation in invasive pituitary adenoma groups (r =0.890, P <0.05; r =0.436, P <0.05). Conclusion The overexpressions of HIF-1α and VEGF protein and mRNA may play important role in invasiveness of pituitary adenomas. [ABSTRACT FROM AUTHOR]