Bilobalide exhibits many biological activities, but its effects on morphine stimulation have not been elucidated. The research aims to explore the function and underlying mechanisms of bilobalide in morphine‐led hippocampal neuron cells. Cells were treated with or without morphine or oxaliplatin (OXA), bilobalide, or SCH772984 dilutions. miR‐101 inhibitor and negative control were transfected into cells. Western blot and quantitative reverse transcription‐polymerase chain reaction were, respectively, conducted to measure the relative expression of proteins or RNAs. Morphine improved the expression levels of orexin1 receptor (OX1R) and c‐FOS, the p/t‐ERK/PKC as well. The c‐FOS protein level and p/t‐ERK/PKC were significantly elevated by morphine + OXA. Bilobalide had no effect on OX1R and p/t‐PKC but evidently decreased the c‐FOS and p/t‐ERK. The p‐ERK and the c‐FOS accumulation levels were remarkably reduced by SCH772984. The production of miR‐101 was promoted by bilobalide but inhibited by the miR‐101 inhibitor. miR‐101 inhibitor abolished bilobalide's inhibitory effects on p/t‐ERK. Bilobalide exhibited morphine‐induced effects on hippocampal neuron cells by upregulating miR‐101.
Objective: It was designed to explore the influence of nano zinc oxide (nano ZnO) on the biological effects of nerve cell PC12, in order to deely make analysis of the effect of nano ZnO on the nervous system. Methods: PC12 cell induced by nerve growth factor (NGF) was the object of study. Methyl thiazolyl tetrazolium assay (MTT) was used to detect the survival rate of cells, fluorescence labeling technique was adopted to detect the content of ROS and flow cytometry was used to make analysis of the proportion of apoptotic cells. Results: After the treatment of PC12 cells by nano ZnO at different concentrations for different time periods, it was found that the survival rate of cells decreased with the concentration increasing and the time extension. It was dependent on the time and concentration. 10 −4 g/ml nano ZnO could decrease the survival rate of PC12 cells remarkably (P < 0.05). The content of reactive oxygen species (ROS) increased with the concentration of nano ZnO rising. Compared with the apoptotic rate of normal cells, 10 −4 g/ml nano ZnO could promote the apoptosis of PC12 cells (P < 0.05). The pretreatment of ROS scavenger could significantly increase the survival rate of PC12 cells (P < 0.05) and inhibit the apoptosis of PC12 induced by nano ZnO (P < 0.05). Conclusions: Nano ZnO could reduce the survival rate of PC12 cells and such an effect was dependent on time and concentration. Besides, nano ZnO could induce the apoptosis of PC12 cells, whose mechanism was related to the increase of ROS content within cells.
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