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AIM: To explore the inhibitory effect and mechanism of compound salvia miltiorrhiza on ovarian cancer by using network pharmacology and molecular docking knowledge. METHODS: The core components of compound salvia miltiorrhiza and the inhibitory effect of compound salvia miltiorrhiza on ovarian cancer cell cycle were studied by combining the methods of MTT cell cycle inhibition and MTT signal network of compound salvia miltiorrhiza. RESULTS: Based on network pharmacology, the core components of compound salvia miltiorrhiza were luteolin and quercetin, and the core target of the disease was VEGFA, SRC, EGFR, hsp90aa1. The docking mode between the core component and the core target EGFR was verified and analyzed by molecular docking. Finally, MTT colorimetry was used to verify that luteolin, one of the core components, significantly inhibited the proliferation of ovarian cancer cells. The results of flow cytometry showed that luteolin induced ovarian cancer A2780 cell cycle arrest in G1/S phase.CONCLUSION: Compound salvia miltiorrhiza preparation can inhibit the proliferation of ovarian cancer cells, which may be related to PI3K Akt signal pathway mediated by EGFR; Network pharmacology and molecular docking technology have important predictability and possibility for the treatment of tumor by compound salvia miltiorrhiza, and have guiding significance for the role and mechanism of compound salvia miltiorrhiza against ovarian cancer cells.
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Objective To investigate the effect of lidocaine on Staphylococcus aureus exotoxin-stimulated peripheral blood mononuclear cells (PBMCs) from patients with atopic dermatitis (AD).Methods Peripheral blood samples were collected from 6 patients with AD,and PBMCs were isolated by a routine method.Then,the PBMCs were stimulated by the Staphylococcus aureus exotoxin toxic shock syndrome toxin-1 (TSST-1) in the absence or presence of lidocaine at varying concentrations.The 3H-TdR incorporation method was performed to detect the proliferation of monocytes,and enzyme-linked immunosorbent assay (ELISA) to quantify the levels of T helper type 1 (Th1) and Th2 cytokines released by PBMCs.Human HaCaT keratinocytes were co-cultured with lidocaine-and TSST-1-stimulated PBMCs from patients with AD for 72 hours,then,Western blot was conducted to examine the expression of filaggrin protein in HaCaT cells.Results TSST-1 (100 μg/L) significantly enhanced the proliferation of PBMCs from patients with AD (stimulation index =75 ± 2.12,P ＜ 0.05),as well as the release of tumor necrosis factor-α (TNF-α),interferon (IFN)-γ,interleukin (IL)-2,IL-12,IL-4,IL-5 and IL-13 by the PBMCs (all P ＜ 0.05).Compared with the blank control group,100 μmol/L lidocaine significantly inhibited the TSST-1-stimulated proliferation of PBMCs from patients with AD (stimulation index =58 ± 3.14,P＜ 0.05),as well as the release of IL-4,IL-5,IL-13,TNF-α and IFN-γ by the stimulated PBMCs (all P ＜ 0.05).Western blot showed that 100 μmol/L lidocaine significantly blocked the down-regulation of filaggrin expression in HaCaT cells (P ＜ 0.01).Conclusion Lidocaine has a significant inhibitory effect on the activation of TSST-1-stimulated PBMCs from patients with AD.