【摘 要】
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OBJECTIVE To investigate the pharmacological effect and mechanism of Sanguisorba officinalis L. (SOL) in non-small cell lung cancer (NSCLC) in vitro and in vivo based on network pharmacology. METHODS Network pharmacology was used to analyze the improving
【机 构】
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School of Pharmacy,Southwest Medical University,Luzhou 646000,China;School of Pharmacy,Southwest Med
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OBJECTIVE To investigate the pharmacological effect and mechanism of Sanguisorba officinalis L. (SOL) in non-small cell lung cancer (NSCLC) in vitro and in vivo based on network pharmacology. METHODS Network pharmacology was used to analyze the improving effect of SOL on NSCLC and possible targets. Cell counting kit 8 (CCK-8) and 5-ethynyl-2\'-deoxyuridine (EdU) staining, Western blotting, flow cytometry of Annexin Ⅴ/PI, Hoechst 33342/PI staining detection and immunofluorescence were utilized in vitro. H&E staining, immunohistochemistry staining and Western blotting were performed in vivo. RESULTS Based on network prediction, we analyzed the 208 common targets of SOL and NSCLC. 36 core targets in 208 common targets were obtained through cytoscape analysis. And the top 10 core targets included Akt, mTOR, EGFR, etc.. KEGG analysis showed that PI3K-Akt signaling pathway was the most likely pathway. Furthermore, the mechanism study found that SOL could activate the PI3K/Akt/mTOR signaling pathway in vitro and in vivo. The anti-proliferative effect of SOL in A549 and H1299 cells was measured and validated by CCK-8 and EdU assay. Immunohistochemical results of Ki67 showed that SOL effectively inhibited tumor growth in vivo. SOL also significantly inhibited the migration and invasion of A549 and H1299 cells. SOL significantly increased the percentage of cells with PI signal in A549 and H1299, and the process of cell death of A549 cells indicated that SOL induced apoptosis. The PARP-1 and caspase-3 in A549 and H1299 were found to be activated in a dose manner. The results in vivo were consistent with those in vitro. CONCLUSION SOL-induced, caspase-3-mediated apoptosis via the induction of the PI3K/Akt/mTOR signaling pathway in NSCLC, which further clarified the mechanism of SOL in the inhibition of NSCLC, and thereby provided a possibility for SOL to serve as a novel therapeutic agent for NSCLC in the future.
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