This study investigates the active components and mechanism of Shufeng Jiedu Capsules (SFJDC) against novel coronavirus through network pharmacology and molecular docking. The TCMSP, TCMID, and BATMAN-TCM databases were used to retrieve the components of SFJDC. The active components were screened by ADME (absorption, distribution, metabolism, and excretion) parameters, and identified by Pubchem, Chemical Book, and ChemDraw softwares. The molecular docking ligands were constructed. SARS Coronavirus-2 Major Protease (SARS-CoV-2-M pro ) and angiotension converting enzyme 2 (ACE2) were used as molecular docking receptors. AutoDock software was used for molecular docking. Cytoscape 3.7.1 software was used to generate an herbs-active components-targets network. Gene Ontology gene function and Kyoto Encyclopedia of Genes and Genomes signal pathway analysis were performed by DAVID data. A total of 1244 components were identified from SFJDC, and 210 active components were obtained. Among them, 97 active components were used as docking ligands to dock with SARS-CoV-2-M pro and ACE2. There were 48 components with good binding activity to SARS-CoV-2-M pro . Ten active components (including 7-Acetoxy-2-methylisoflavone, Kaempferol, Quercetin, Baicalein, Glabrene, Glucobrassicin, Isoglycyrol, Wogonin, Petunidin, and Luteolin) combined with SARS-CoV-2-M pro and ACE2 simultaneously. Among them, Kaempferol, Wogonin, and Baicalein showed higher binding activity. The herbs-active components-targets network contained 7 herbs, 10 active components, and 225 targets. The 225 target targets were involved in 653 biological processes of Gene Ontology analysis and 130 signal pathways (false discovery rate ≤ 0.01) of Kyoto Encyclopedia of Genes and Genomes analysis. The active components of SFJDC (such as Kaempferol, Wogonin, and Baicalein) may combine with ACE2 and act on multiple signaling pathways and targets to exert therapeutic effect on novel coronavirus.
Cydonia oblonga miller (quince) plant serves as a potential folk medicine for treating hypertension and cardiovascular diseases in China. However, to the best of our knowledge, no study has been conducted on the polyphenolic profile and anti-adipogenic effect of quince fruit grown in China. In the current study, we aimed to investigate the quince fruit extract’s major phenolic compounds, evaluate their antioxidant activity, and examine their effect on adipogenesis in 3T3-L1 cells. A rapid and sensitive analytical method was established for the simultaneous determination of major polyphenolic compounds by using ultra-pressure liquid chromatography coupled with a triple quadrupole mass spectrometer (UPLC-MS/MS). Among the 10 compounds, the cryptochlorgenic acid was noticed as the most abundant compound of both purified (242.44 ± 0.73 µg/mg dw) and unpurified extract (3.37 ± 0.01 µg/mg dw) followed by quercetin 3-rutinoside and chlorogenic acid. Alternatively, both extracts possessed a high quantity of phenolic acids (purified extract = 483.10 ± 5.16 µg/mg dw and unpurified extract = 7.89 ± 0.02 µg/mg dw). The purified extract exhibited a strong antioxidant capacity (DPPH: EC50 = 3.316 µg/mL, ABTS: EC50 = 36.38 µg/mL) as compared to the unpurified extract. Additionally, our results also showed that the extract at 100 µg/mL significantly suppressed the preadipocyte differentiation and decreased the lipid droplets up to 69% in mature adipocytes. The present study highlights an accurate and fast detection method for quince fruit extract polyphenolic compounds with its antioxidant and antiadipogenic effects. The study also provides the necessary information for the rational development and utilization of quince fruit extract as a source of phytochemicals.
Background: Lung adenocarcinoma (LUAD) has high morbidity and is prone to recurrence. TIMELESS (TIM), which regulates circadian rhythms in Drosophila, is highly expressed in various tumors. Methods: We used tumor samples from patients with lung carcinoma and LUAD patient data from public databases to confirm the relationship of TIM expression with lung cancer. We used NSCLC cell lines and siRNA to knock down TIM expression, and further analyzed cell proliferation, migration and colony formation. By using western blot and qPCR, we detected the influence of TIM on EGFR, Sphk1 and AMPK. With proteomics analysis, we comprehensively inspected the different changed proteins influenced by TIM and did global bioinformatic analysis. Results: In this study, we found that TIM expression was elevated in LUAD and that this high expression was positively correlated with more advanced tumor pathological stages and shorter overall and disease-free survival. Moreover, gefitinib efficacy in patients with LUAD could be influenced by TIM expression, and the antitumor effect of gefitinib was significantly improved with TIM knockdown. TIM knockdown inhibited epidermal growth factor receptor (EGFR) activation and phosphorylation of its downstream AKT/mTOR and ERK1/2 pathways. We also clarified that TIM regulated the activation of sphingosine kinase 1 (SPHK1) in LUAD cells, while SPHK1 knockdown inhibited EGFR activation. Quantitative proteomics techniques combined with bioinformatics analysis were adopted to clarify the global molecular mechanisms regulated by TIM in LUAD. The results of proteomics suggested that mitochondrial translation elongation and termination were altered, which were closely related to the process of mitochondrial oxidative phosphorylation. Knockdown of TIM reduced the ATP content and promoted AMP-activated protein kinase (AMPK) activation. Conclusions: Our study revealed that TIM could regulate EGFR activation through AMPK and SPHK1, as well as influence mitochondrial function and alter the ATP level; thus, TIM is a key factor in LUAD.
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