ABSTRACT
Objective:To explore the molecular mechanism of Polygalae Radix - Acori Tatarinowii Rhizoma medicinal pair for depression and Alzheimer disease (AD) with the same treatment through network pharmacology. Methods:Effective components of Polygalae Radix - Acori Tatarinowii Rhizoma medicinal pair were retrieved from TCMSP, TCMID and ETCM databases. The disease targets of depression and AD were retrieved from GeneCards, TTD and CTD databases. Targets of action of drugs on active components were predicted through SwissTargetPrediction, and then the intersection targets of medicinal pair and the diseases were taken. Cytoscape 3.6.1 was used to construct the interaction network of Polygalae Radix - Acori Tatarinowii Rhizoma medicinal pair on "component-common target-disease". The enrichment analysis of GO function and KEGG pathway was carried out with the help of Metascape platform, and molecular docking verification was carried out. Results:Through searching the databases and literature, 78 compounds in Polygalae Radix - Acori Tatarinowii Rhizoma medicinal pair were obtained, corresponding to 41 targets of different diseases with the same treatment. The GO function was mainly concentrated in response to lipopolysaccharide and cellular response to nitrogen compound. The KEGG pathway was mainly concentrated in lipid and atherosclerosis, calcium signaling pathway, serotonergic synapse, insulin resistance and so on. The core targets were PTGS2, ESR2, etc. Molecular docking showed that most of the core components could form stable conformation with the core targets. Conclusions:Polygalae Radix - Acori Tatarinowii Rhizoma medicinal pair has the characteristics of multi-component, multi-target and multi-pathway in the same treatment of depression and AD. Through their core components of senegenin, 1-carbobutoxy-β-carboline, 6-hydroxy-1,2,3,7-tetramethoxyxanthone, kaempferol and etc., the pair can act on PTGS2 and other targets, regulate lipid and atherosclerosis, calcium signaling pathway, serotonergic synapse, insulin resistance and so on, and play a therapeutic role in depression and Alzheimer's disease with the same treatment.
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Objective To study the effect of Angelicin on proliferation activity and anti-aging related protein expression of human HDF cells and its mechanism. Methods According to the random number table method, the cells were divided into blank group, model group, estradiol group, Angelicin group, estrogen receptor antagonist+estradiol group, estrogen receptor antagonist+Angelicin group, and P38 pathway blocker group. Different groups were given the according drugs respectively for 24 h. Except the blank group, all the groups of cells were given UVB irradiation with a dose of 150 mJ/cm2. The MTT assay was used to detect cell proliferation rate. The Western blot was used to detect the expression levels of COLⅠ, MMP-1, ERβ, P38 and p-P38 in cells, and the MMP-1 mRNA expression was detected by real-time fluorescent quantitative PCR.Results Compared with the model group, the proliferation rate of HDF cells significantly increased in Angelicin(10,1,0.1 and 0.01 μmol/L groups)(P<0.01);The protein expression of COLⅠ (0.326 ± 0.006 vs. 0.176 ± 0.007),ERβ(0.281 ± 0.011 vs.0.143 ± 0.006)significantly increased(P<0.01),and the expression of MMP-1(0.256 ± 0.006 vs.0.395 ± 0.006)and p-P38(0.224 ± 0.003 vs.0.318 ± 0.005)significantly decreased (P<0.01) in Angelicin 10 μmol/L group. Compared with 10 μmol/L Angelicin group, the protein expression of estrogen receptor antagonist+Angelicin group ERβ(0.120 ± 0.007 vs.0.281 ± 0.011)significantly decreased and MMP-1mRNA(1.377 ± 0.012 vs.1.024 ± 0.010)significantly increased(P<0.01).Conclusions The Angelicin may degrade MMP-1 through the ER-P38 MAPK signaling pathway,and then promote collagen synthesis, to achieve the purpose of prevention and treatment of photoaging.
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Objective To study the effect of psoralen isoflavone on the treatment of PC12 cells injured by Aβ and the mechanism on the effect of the psoralen isoflavones on the expression of related proteins. Methods The PC12 cells were divided into blank group, model group, E2 group, and psoralen isoflavones group by random number table method, In addition to the blank group the rest of each group culture medium were added 20μmol/L of Aβ25-35 modeling, The E2 group was added to the 10-3μmol/L oestrogen and psoralen isoflavones group for the intervention of 102-10-6 μmol/L.The proliferation rate of PC12 cells was detected by MTT assay, and the expression of APP, BACE1, ERβ, p-ERK and Aβ protein was detected by Western Blot. Results Compared with the model group, the proliferation of PC12 cells induced by 10-1μmol/L of psoralen isoflavone increased (101％ vs. 52％, P<0.01); The expression of p-ERK (0.751± 0.066 vs. 0.364 ± 0.015), ERβ(0.756 ± 0.105 vs. 0.337 ± 0.045) increased significantly (P<0.01); APP (0.382 ± 0.039 vs. 0.479 ± 0.015), BACE1 (0.517 ± 0.024 vs. 0.622 ± 0.029), Aβ (0.430 ± 0.032 vs. 0.581 ± 0.030) expression amount were significantly lower (P<0.05). Conclusions Psoralen isoflavones have a certain therapeutic effect on PC12 cells injured by Aβ.