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Epigenetics and postsurgical ache: A new scoping evaluation.
The activities of Caspase-3 and Caspase-9 were increased significantly (P＜0.05), while the mitochondrial membrane potential was decreased significantly (P＜0.05). In addition, the mRNA and protein expression levels of Bax, Cyt c and APAF-1 were increased significantly (P＜0.05), while the mRNA and protein expression levels of Bcl-2 were decreased significantly (P＜0.05). Conclusion Toosendanin up-regulates the expressions of Bax, Cyt c and APAF-1, down-regulates the expression of Bcl-2 gene, enhances the activities of caspase-3 and caspase-9, and induces the apoptosis of human gastric cancer MGC-803 cells.Objective To investigate the effect of betulinic acid on the proliferation of human gastric cancer MGC-803 cells in vitro. Methods Human gastric cancer MGC-803 cells were divided into 4 groups, each with 3 multiple holes. Control cells add betulinic acid at a concentration of 0 μg /ml, and the other three experimental groups were added with final concentration of 10, 20, 30 μg/ml Betulinic acid respectively. Cells in each group were incubated in a 5% CO2 incubator for 48 hours, and the Giemsa staining method and trypan blue exclusion method were used to detect the effect of betulinic acid on the cell clone formation rate and growth inhibition rate; EdU method and flow cytometry were used to detect cell proliferation and cell cycle changes; qRT-PCR and Western blot were used to detect the expressions of cell cycle regulators CCNB1 and CCND1. Results Compared with the control group, the clone formation rate of human gastric cancer MGC-803 cells was significantly reduced (P＜0.01), the growth inhibition rate was significantly increased, and the cell proliferation ability was significantly decreased (P＜0.01); with the increase of betulinic acid concentration in each experimental group the proportion of cells in the G1 phase was gradually decreased, and the number of cells in S phase was increased significantly (P＜0.01); the mRNA and protein expression levels of cell cycle regulators CCNB1 and CCND1 were decreased significantly, and the 30 μg/ml betulinic acid treatment group performed best. Conclusion At a final concentration of 10～30 μg/ml, betulinic acid can reduce the proliferation of human gastric cancer MGC-803 cells, inhibit cell growth, and down-regulate the expression of CCNB1 and CCND1 to block human gastric cancer MGC-803 cells in the S phase.Objective In this study, human gastric cancer MGC-803 cells were treated with betulinic acid at different concentrations to investigate its effect on cell autophagy. Methods The human gastric cancer MGC-803 cells were divided into 4 groups, each group was set with 3 replicate. The control group was not treated with betulinic acid, the other three groups were added with final concentration of 10,20,30 mg/L betulinic acid, respectively. Cells were treated with betulinic acid for 48 h,qRT-PCR was applied to detect the effect of betulinic acid on mRNA expressions of autophagy-related genes in human gastric cancer MGC-803 cells. Western blot was performed to determine the protein expressions of cell autophagy-related genes after drug treatment. Immunofluorescence was used to detect the localization and expression of LC3 protein in MGC-803 cells after drug treatment. Results Compared with the control group,in the concentration range of 10~30 mg/L, the mRNA expression of LC3 and Beclin-1 in human gastric cancer MGC-803 cells treated with betulinic acid were increased significantly, the expressions of Beclin-1 and LC3-Ⅱ protein were also increased significantly, while the expression of LC3-Ⅰ protein was decreased significantly. Among them, betulinic acid at the concentration of 30 mg/L showed the best effects. In addition, betulinic acid induced the LC3 protein in MGC-803 cells to form spot aggregates in the cytoplasm. Conclusion At the concentrations of 10~30 mg/L, betulinic acid can induce autophagy in human gastric cancer MGC-803 cells.Objective This article mainly studies the effects of miR-125b-5p on the proliferation and apoptosis of human hemangioma endothelial cells HemECs. Methods RT-qPCR was used to detect the expressions of miR-125b-5p and MCL-1 mRNA in HemECs and collateral cells of human hemangioma endothelial cells. HemECs were selected and divided into control group, miR-NC group, miR-125b-5p mimic group, miR-125b-5p inhibitor group, pc-MCL-1 group, miR-125b-5p+ pc-MCL-1 group, 9 multiple holes in each group. . HemECs were transfected with 100 nmol · L-1 of miR-NC, miR-125b-5p mimic, miR-125b-5p inhibitor, pc-MCL-1 plasmids separately or in combination. MTT method was used to detect the proliferation of HemECs. The apoptosis of HemECs was detected by flow cytometry. Dual luciferase report was used to to detect targeting relationship. The relative expression levels of Ki67, PCNA, cleaved caspase-3, Bax, Bcl-2, p-p70s6k/ p70s6k, p-AKT/AKT, and p-mTOR/mTOR proteins were detected by Western blot. Results By comparing the expression s and the expressions of Ki67 and PCNA in miR-125b-5p+ pc-MCL-1 group were increased significantly (P＜0.01), the apoptosis rate of HemECs and the expressions of cleaved Caspase-3 and Bax were decreased significantly, while the expression of Bcl-2 was increased (P＜0.01). The expressions of p-AKT/AKT, p-mTOR/mTOR, and p-p70S6K/p70S6K was also increased significantly (P＜0.01). Conclusion miR-125b-5p inhibits the proliferation of human hemangioma endothelial cells and induces apoptosis. The mechanism may be related to the targeted down-regulation of MCL-1 expression and inhibition of AKT/mTOR pathway activation.Objective To investigate the effects of novel BimunoGalactooligosaccharides (B-GOS) on cognitive behavior and depression of APP/PS1/tau Alzheimer's disease transgenic mice. Methods Five-month-old male APP/PS1/tau AD transgenic mice and C57BL/6J control mice were divide into C57+Vehicle group, C57+B-GOS group, APP/PS1/tau+Vehicle group and APP/PS1/tau+B-GOS group, with 10 mice in each group. After continuous administration of B-GOS for 5 months, the cognitive behavior and depressive mood changes of mice in each group were detected by open field experiment, new object recognition experiment, Y maze experiment, Morris water maze experiment, tail suspension test, forced swimming test and conditioned fear experiment, respectively. Results ①Open field experiment the percentage of activity time in the central area of open field in APP/PS1/tau+Vehicle group mice was significantly lower than that in C57+Vehicle group mice (P＜0.01), and was remarkably increased after B-GOS intervention (P＜0.05). ② New object recognitiing test the percentage of immobility time in APP/PS1/tau+Vehicle group mice was dramatically higher than that in C57+Vehicle group mice (P＜0.01), and was obviously reduced after B-GOS intervention (P＜ 0.01). ⑥ Conditioned fear experiment before conditioned stimulus (CS), the freezing ratio of mice in each group had no statistical difference (P＞0.05). After CS, the freezing ratio of APP/PS1/tau+Vehicle group mice was significantly lower than that of C57+Vehicle group mice (P＜0.01), and was notably increased after B-GOS intervention (P＜0.01). Conclusion B-GOS could reverse the cognitive behavioral impairment of APP/PS1/tau mice and alleviate their depression to a large extent.Objective To compare epicardial electrograms between the left atrium (LA) and pulmonary veins (PVs) dynamically at development of persistent atrial fibrillation(AF) in goats PVs. Methods Ten female goats were instrumented with electrodes at the LA and left side PV. Sustained AF (＞24 h) was induced in the goat by rapid intermittent left atrial pacing for(9.5±2.3)days at a pacing interval of 20 ms for 1 s with a maximum output of 6.0 V, followed by a 2-s period without pacing. Characteristics of PVs and LA epicardial electrograms were analyzed in the development of AF. Results With prolonged stimulation, the duration of AF was prolonged, complex fractionated atrial electrograms(CFAEs) in LA and was increased gradually, PVs had more CFAEs than LA all the time. When induced AF lasted for more than 24 h, CFAEs in PVs became sustained approximately (2.7%±3.6% vs 92.6%±6.4%, at onset of AF vs AF lasted for more than 24 h, P＜0.05), and the ratio of CFAEs in PVs was more than that in LA (92.6%±6.4% vs 72.8%±5.3%, P＜0.05). Conclusion The epicardial CFAEs are in specific area, which increase along with electrical remodeling. The epicardial CFAEs may play an important role in the maintenance of AF in this model.Objective To investigate the obestatin neural projections from arcuate nucleus (ARC) to hippocampus in diabetic rats, and its effects on gastric motility and gastric emptying of rats. Methods Diabetic model was established by fructose intake combined with streptozotocin injected intraperitoneally in healthy male Wistar rats. Diabetic rats were randomly divided into five groups control group (NS group), 0.1, 1 and 10 pmol obestatin group, and obestatin + NBI27914 group, with 7 rats in each group. 0.5 μl saline (NS), obestatin (0.1 pmol, 1 pmol, 10 pmol) or the mixture (10 pmol obestatin + 60 pmol NBI27914) was injected into the hippocampus respectively, the gastric motility was recorded immediately after administration, and the gastric emptying was studied 15 min later. ARC-hippocampus obestatin neural pathway and ARC obestatin mRNA expression were compared between normal and diabetic rats with fluorogold (FG) retrograde tracing and immunofluorescence histochemical staining. Results Compared with normal rats, the number of ARC FG/obestatin double labeled neurons and the expression level of ARC obestatin mRNA were decreased significantly in diabetic rats (P＜0.05); Obestatin could inhibit gastric motility and gastric emptying in a dose-dependent manner (P＜0.05~0.01) and the effects of obestatin could be partially blocked by NBI27914, an antagonist of corticotropin releasing factor receptor 1 (CRFR1) (P＜0.05). Compared with normal rats, the inhibitory effects of obestatin on gastric motility and gastric emptying were significantly decreased in diabetic rats (P＜0.05). Conclusion There is an obestatin neural pathway between ARC and hippocampus, which participates in the regulation of gastric motility and gastric emptying in diabetic rats, and CRFR1 signal pathway is involved in this process. The damage of this neural pathway may participate in gastric motility dysfunction in early stage of diabetes.Objective To investigate the relationship between mitochondrial DNA (mtDNA) variation and high altitude essential hypertension(HAEH) in the Chinese Tajik population. Methods Fifty-three patients with HAEH and 46 healthy subjects were enrolled from the Chinese Tajik population. The mtDNA fragments were amplificated by polymerase chain reaction, and products were sequenced to acquire full sequence of mtDNA. BTK inhibitor in vivo The mtDNA sequences of all subjects were compared to the Cambridge sequence to explore mtDNA variations and analyze difference between HAEH and healthy controls. Online softwares were applied to predict function changes caused by positive associated mtDNA variations. Results Compared to the control group, the frequency of haplogroup U4b was significant higher in HAEH group(P=0.023,OR=7.062,CI(95%)=1.306-38.182), and the frequencies of 8 mutations from haplogroup U4b showed a significant difference between the HAEH group and control group (all with P values below 0.05). The mt DNA15693T＞C mutation was the only missense mutation, which affected amino acid 316 in mitochondrial cytochrome b (MTCYB) by changing it from methionine to threonine.
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