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05), while the GSH, PI3K, p-Akt and mTOR levels were significantly increased (P<0.05). Conclusion This study proves that linagliptin exerted a neuroprotective effect in I/R mice, which may be mediated by activation of the PI3K/AKT/mTOR pathway.Objective To investigate the effects of Ganmai Dazao Tang on behavior and monoamine neurotransmitters in rats with depression, and to explore its potential mechanism from synaptic structure. Methods Sixty SD rats were randomly divided into 5 groups normal control group, model group, fluoxetine group (10.8 mg/kg), Ganmai Dazao Tang high and low dose group (9.72, 4.86 g/kg), 12 rats in each group. Except the control group, the rats in the other groups were all chronically unpredictable mild stress (CUMS) to establish a depression model, and were treated by intragastric administration for 21 days. The depression-like behaviors of rats were evaluated by sucrose consumption test and open field test. The contents of serotonin (5-HT) and norepinephrine (NE) in hippocampus were detected by ELISA. The synaptic damage of neurons was observed by Golgi staining. The synaptic structure protein expression levels of MAP-2 and GAP-43 of hippocampus were detected by Immunohistochemistry and Western blot. Results Compared with control group, the sucrose preference and autonomic activity scores of the depression model rats were decreased significantly (P<0.01), the levels of 5-HT and NE in hippocampus were decreased significantly (P<0.01), and the dendritic spines were absent, and the expressions of MAP-2 and GAP-43 were down-regulated significantly (P<0.01). After treated with Ganmai Dazao Tang, the depression-like behavior of the model rats was significantly relieved (P<0.01), and the levels of 5-HT and NE were increased (P< 0.05). Dendritic spine density, length and branching were increased, the expressions of MAP-2 and GAP-43 were increased (P< 0.01). Conclusion Ganmai Dazao Tang can improve the depression-like behavior of depression model rats and increase the monoamine neurotransmitter content in hippocampus, which may be related to up-regulation of synaptic structural proteins and relief of synaptic damage in neurons.Objective To investigate the effects of fatty acid binding protein 5(FABP5)- peroxisome proliferator-activated receptor gamma(PPARγ) signaling pathway on learning-memory ability and lipid metabolism in rats with vascular dementia(VD) and its mechanisms. Methods ①VD model rats were established by ligating bilateral common carotid artery. These rats were divided into three groups normal group (WT group), sham-operated group (sham group) and VD model group; ②WT group and FABP5 inhibitor group were set up. After four weeks, Morris water maze test was used to detect spatial learning and memory ability in rats. RT-qPCR and Western blot methods were used to detect the expressions of FABP5, PPARγ, p-PPARγ and lipoprotein lipase (LPL) in the brain at the mRNA and protein levels. The levels of TC, TG and FFA in the brain were detected by assay kits. Results Compared with the WT group and sham group, the learning-memory ability of the VD model and the FABP5 inhibitor group were significantly decreased, and the expressions of FABP5, PPARγ, p-PPARγ and LPL were significantly decreased at mRNA level and protein level in the brain; and the levels of TC, TG and FFA were increased significantly in the brain. Conclusion FABP5 can affect the learning-memory ability and lipid metabolism in VD rats through PPARγ and LPL.Objective To investigate the effects of simulated hypoxia environment at an altitude of 5 500 meters on hypothalamic-pituitary-thyroid (HPT) axis and intestinal flora of rats and the correlation between them. Methods The hypoxia model of adult male SD rats was established by hypobaric chamber with simulated altitude of 5 500 m. The hypoxia groups were set for 1, 3, 7, 14, 21 and 28 days, and the normoxic recovery group were set for 1 and 3 days after hypoxia (8 rats per group, hypoxia time 24h per day). Daily body weight and food intake of rats were recorded. https://www.selleckchem.com/products/beta-aminopropionitrile.html The serum levels of HPT axis hormones were detected by enzyme-linked immunosorbent assay (ELISA). Intestinal flora was analyzed by 16s rDNA sequencing. The correlation between intestinal flora and serum HPT axis hormone was analyzed by Spearman correlation analysis. Results Compared with the normoxic group, the body weight and food intake were significantly reduced (P<0.01). In the 1-day and 3-day groups, the levels of thyrotropin releasing hormone (TRH)lated with TRH and TSH (P< 0.05), Prevotella, Bacteroides, Odoribacter and Parabacteroides were significantly correlated with TSH, TT4, TT3 and FT4 (P< 0.05), respectively. Lactobacillus was significantly correlated with TRH, TSH and FT4 (P<0.05). Akkermansia was significantly correlated with TRH and FT4 (P<0.05). RC4-4 was significantly associated with TSH and TT3 (P<0.05). Conclusion Hypoxia stress at an altitude simulating 5500 meters significantly changed the composition of the intestinal flora of SD rats. This may be a change in thyroid function adapted to the hypoxia environment, and the degree of change is related to the time of hypoxia stress. The change of intestinal microflora is significantly correlated with the hormone level of HPT axis.Objective To investigate the sensitivity of carotid body to hypoxia and the effect of dopamine on the sensitivity of carotid body to hypoxia after acute intermittent hypoxia stimulation in rats. Methods The isolated carotid body-sinus nerve in rat was transferred to incubator, and then the isolated sinus nerve was inhaled into the recorded glass electrode for recording electrical signals. The baseline buffer was bubbled with 95% O 2 + 5% CO 2 mixture gas, and the hypoxic stress was treated with 5% O 2 + 5% CO 2 + 90% N2 mixture gas, hypoxic stimulation was given for 30 seconds, 95% O 2 + 5% CO 2 for 90 seconds, a total of 10 cycles. No less than 5 rats in each group. Results In this experiment, the electrical activity of sinus nerve isolated from rats was enhanced by hypoxia stimulation after acute intermittent hypoxia, but the response of sinus nerve to hypoxia was inhibited by dopamine. Before acute intermittent hypoxic stress, dopamine also inhibited the firing activity of sinus nerve, but after acute intermittent hypoxic cycle, the inhibition of dopamine on the firing activity of sinus nerve was strengthened.
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