This study aimed to analyze the function and latent mechanism of long noncoding RNA BACE1-antisense transcript (lncRNA BACE1-AS) in MPP+-induced SH-SY5Y cells. SH-SY5Y cells were cultivated in 1 mM MPP+ for 24 h to establish Parkinson's disease (PD) model in vitro. TargetScan and luciferase reporter assay were conducted to predict and verify the interaction between microRNA (miR)-214-3p and CDIP1 (Cell death-inducing p53-target protein 1). Cell viability, lactate dehydrogenase (LDH) release, and cell apoptosis were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2 H-tetrazolium bromide (MTT), LDH, and flow cytometer. The secretion of inflammatory factors and representative biomarkers of oxidative stress, including reactive oxygen species (ROS) and superoxide dismutase (SOD) were assessed using enzyme-linked immunosorbent assay (ELISA) and specific assay kits. Results suggested that lncRNA BACE1-AS was over-expressed and miR-214-3p was under-expressed in MPP+-stimulated SH-SY5Y cells. Further analyses revealed that MPP+ inhibited cell viability; enhanced cell apoptosis, Cleaved Caspase-3 expression and Cleaved Caspase-3/GAPDH ratio; induced oxidative stress and inflammation in SH-SY5Y cells were inhibited by lncRNA BACE1-AS-siRNA transfection; and all these inhibitions were reversed by miR-214-3p inhibitor. In addition, we found that CDIP1 was directly targeted by miR-214-3p and up-regulated in MPP+-stimulated SH-SY5Y cells. Further functional assays suggested that CDIP1-plasmid reversed the effects of miR-214-3p mimic on MPP+-stimulated SH-SY5Y cells. In conclusion, lncRNA BACE1-AS regulates SH-SY5Y cell proliferation, apoptosis, inflammatory response, and oxidative stress through direct regulation of miR-214-3p/CDIP1 signaling axis, and could be a potential candidate associated with the diagnosis and treatment of PD.
A combined high-pressure carbon dioxide (HP-CO2) and thermal degradation reaction of betanin and isobetanin in aqueous solution was investigated and can be described by a first-order decay. At 45 °C, the degradation rate constant (k) for each pigment component significantly increased (the half-life (t1/2) decreased, p < 0.05) with elevated pressure. Furthermore, HP-CO2 treatment led to lower k values (higher t1/2 values) than thermal treatment. However, k and t1/2 values approached those of thermal treatment when the pressure was >30 MPa combined with temperatures exceeding 55 °C. Moreover, betanin was more stable than isobetanin under HP-CO2. Ea values ranged from 94.01 kJ/mol for betanin and 97.16 kJ/mol for isobetanin at atmospheric pressure to 170.83 and 142.69 kJ/mol at 50 MPa, respectively. A higher pressure and temperature as well as longer exposure time resulted in higher values of L*, b*, C*, and h°. HP-CO2 induced more degradation products from betanin and isobetanin than thermal treatment with an identical temperature and exposure time.
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