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Aim To study and verify the effeet and po¬tential mechanism of punicalagin ( Pun) in the treat-ment of depression by preliminary experiments based on network pharmacology.Methods The intersection genes of Pun and depression were obtained through the database, and protein interaction ( PPI ), GO and KEGG were enriched and analyzed.Molecular docking technology was used to preliminarily verify the binding ability of Pun active components to core therapeutic targets.The depression model of CUMS mice was es¬tablished by chronic stress, and Pun was administered by gavage.Open field experiments were conducted to investigate behavior changes.The content of neuro¬transmitters in hippocampus was detected by liquid chromatography-mass spectrometry ( LC-MS / MS ).Results The results of network pharmacology showed that Pun had 76 targets involved in the occurrence of depression, and PPI network showed that the intersec¬tion genes were closely related.Proteoglycans, lipids and atherosclerosis enriched in cancer.The results of molecular docking showed that there was a good bind¬ing between the compound and the target protein.The results of animal experiments showed that Pun could in¬crease the exploration desire of open field experimental mice.The levels of DA and 5-HT in hippocampus in-creased ( P < 0.05, P < 0.01 ).Conclusions Pun can significantly reduce the depressive state of mice, and its mechanism may act on ALB and AKT1 targets, mediate proteoglycans, lipids and atherosclerotic path¬ways in cancer, so as to improve the secretion of neu¬rotransmitters.
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Objective To measure the dynamic parameters of pushing manipulation with one-finger (PMOF), and provide the quantitative basis for evaluation and measurable criteria of PMOF. Methods A multi-film pressure measurement system was used to test and record the graphics of the operator when performing PMOF, and the data of corresponding parameters were recorded and analyzed. Results For PMOP, the maximum force was (11.75±0.88) N, the operation frequency was (111.7±6.98) times/ min, the cycle was (539±35.73) ms, the effective work ratio was greater than 0.28, and the waveform homogeneity was greater than 0.927. Conclusions The requirement of being permanent, forceful, homogeneity during PMOP can be objectively measured thorough graphics and quantitative indicators, but there is still a lack of quantitative indicators to measure and evaluate the requirement of being soft, deep and thorough for PMOF.
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<p><b>UNLABELLED</b>OBJECTIVE To observe the changing laws of the protein expression of N-methyl D-aspartate receptor (NMDAR) in rat hippocampal subfields following focal ischemia/reperfusion injury, and to study the effects of sodium tanshinone B (STB) on it, thus exploring the possible mechanism of STB for treating cerebral ischemia.</p><p><b>METHODS</b>The rat model of focal cerebral ischemia/reperfusion injury was established using middle cerebral artery occlusion (MCAO) by reversibly inserting a nylon thread. The Wistar rats were randomly divided into the sham-operation group, the I/R model group, and the low, middle, and high dose STB groups. The neural functional disturbance was scored referring to the 5-grade Zea Longa EL standard. The protein expression of NMDAR1 in the ischemic side was detected using immunohistochemical assay.</p><p><b>RESULTS</b>There was statistical difference in the scores of the neural functional disturbance in the middle and high dose STB groups when compared with the model group (P < 0.01). Results of the immunohistochemical assay showed the expression of NMDAR1 in CA1 region was obviously higher in the I/R model group, the low and middle dose STB groups than in the sham-operation group (P < 0.01). The expression of NMDAR1 in CA1 region was obviously lower in the high dose STB group than in the I/R model group (P < 0.01), the low (P < 0.01) and middle dose STB groups (P < 0.05). The expression of NMDAR1 in CA3 region was obviously higher in the low dose STB group and the I/R model group than in the sham-operation group, the middle and high dose STB groups (P < 0.01). The expression of NMDAR1 in CA3 region was obviously higher in the high and middle dose STB groups than in the sham-operation group (P < 0.05).</p><p><b>CONCLUSIONS</b>STB could promote the recovery of neural functions in cerebral ischemia/reperfusion injury rats. STB fought against cerebral ischemia/reperfusion injury by lowering excitable neurotransmitter glumatic acid and reducing the protein expression of NMDAR1.</p>