Abstract
["This study was to investigate the protective effect of paeoniflorin (PF) on hydrogen peroxide-induced injury. Firstly, \"SMILES\" of PF was searched in Pubchem and further was used for reverse molecular docking in Swiss Target Prediction database to obtain potential targets. Injury-related molecules were obtained from GeenCards database, and the predicted targets of PF for injury treatment were selected by Wayne diagram. For mechanism analysis, the protein-protein interactions were constructed by String, and the KEGG analysis was conducted in Webgestalt. Then, cell viability and cytotoxicity assay were established by CCK8 assay. Also, the experimental cells were allocated to control, model (200 \u03bcmol\u00b7L HO), SB203580 10 \u03bcmol\u00b7L (200 \u03bcmol\u00b7L HO+ SB203580 10 \u03bcmol\u00b7L), PF 50 \u03bcmol\u00b7L (200 \u03bcmol\u00b7L HO+ PF 50 \u03bcmol\u00b7L), and PF 100 \u03bcmol\u00b7L (200 \u03bcmol\u00b7L HO+ PF 100 \u03bcmol\u00b7L) groups. We measured the intracellular ROS, Hoechst 33258 staining, cell apoptosis, the levels of Bcl-xl, Bcl-2, Caspase-3, Cleaved-caspase3, Cleaved-caspase7, TRPA1, TRPV1, and the phosphorylation expression of p38MAPK. There are 96 potential targets that may be associated with PF for injury treatment. Then, we chose the \"Inflammatory mediator regulation of TRP channels\" pathway for the experimental verification from the first 10 KEGG pathway. In experimental verification, HO decreased the cell viability moderately (P < 0.05), and 100 \u03bcmol\u00b7L PF increased the cell viability significantly (P < 0.05). Depending on the difference of intracellular ROS fluorescence intensity, PF inhibited H O-induced reactive oxygen species production in Schwann cells. In Hoechst 33258 staining, PF reversed the condensed chromatin and apoptotic nuclei following HO treatment. Moreover, Flow cytometry results showed that PF could substantially inhibit HO induced apoptosis (P < 0.05). Pretreatment with PF obviously reduced the levels of Caspase3, Cleaved-caspase3, Cleaved-caspase7, TRPA1, TRPV1, and the phosphorylation expression of p38MAPK after H O treatment (P < 0.05), increased the levels of Bcl-2, and Bcl-xl ( P < 0.05). PF inhibited Schwann cell injury and apoptosis induced by hydrogen peroxide, which mechanism was linked to the inhibition of phosphorylation of p38MAPK.",{"copyright":"Copyright \u00a9 2021 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved."}]
