Based on network pharmacology and molecular docking to explore the protective effect of Epimedii Folium extract on cisplatin-induced intestinal injury in mice

Abstract

Background: Epimedii Folium, as a natural botanical medicine, has been reported to have protective effects on intestinal diseases by modulating multiple signaling pathways. This study aimed to explore the potential targets and molecular mechanisms of Epimedii Folium extract (EFE) against cisplatin-induced intestinal injury through network pharmacology, molecular docking, and animal experiments.Methods: Network pharmacology was used to predict potential candidate targets and related signaling pathways. Molecular docking was used to simulate the interactions between significant potential candidate targets and active components. For experimental validation, mice were intraperitoneally injected with cisplatin 20 mg/kg to establish an intestinal injury model. EFE (100, 200 mg/kg) was administered to mice by gavage for 10 days. The protective effect of EFE on intestinal injury was analyzed through biochemical index detection, histopathological staining, and western blotting.Results: Network pharmacology analysis revealed that PI3K-Akt and apoptosis signaling pathways were thought to play critical roles in EFE treatment of the intestinal injury. Molecular docking results showed that the active constituents of Epimedii Folium, including Icariin, Epimedin A, Epimedin B, and Epimedin C, stably docked with the core AKT1, p53, TNF-α, and NF-κB. In verified experiments, EFE could protect the antioxidant defense system by increasing the levels of glutathione peroxidase (GSH-Px) and catalase (CAT) while reducing the content of malondialdehyde (MDA). EFE could also inhibit the expression of NF-κB and the secretion of inflammatory factors, including TNF-α, IL-1β, and IL-6, thereby relieving the inflammatory damage. Further mechanism studies confirmed that EFE had an excellent protective effect on cisplatin-induced intestinal injury by regulating PI3K-Akt, caspase, and NF-κB signaling pathways.Conclusion: In summary, EFE could mitigate cisplatin-induced intestinal damage by modulating oxidative stress, inflammation, and apoptosis.

Integrating UPLC-Q-Orbitrap MS with serum pharmacochemistry network and experimental verification to explore the pharmacological mechanisms of Cynanchi stauntonii rhizoma et radix against sepsis-induced acute lung injury

“…In this work, the main active components of Csrer were analysed by UPLC-Q-Orbitrap MS. Network analysis was then used to predict targets and pathways. Moreover, molecular docking and simulations can predict ligand-receptor interactions and binding capacity (Tong et al, 2021;Hou et al, 2022;Wang et al, 2022;Xia et al, 2022). Furthermore, we verified the pharmacologic and mechanism of Csrer on LPS-induced ALI/ARDS in mice experiments.…”

“…Oxidative stress and ROS overexpression are essential for developing ALI (Zhang et al, 2021;Liang et al, 2022a). Based on previous studies, SOD and MDA are critical enzymes in maintaining ROS balance (Xia et al, 2022). In the present study, ELISA was used to detect the activities of ROS, SOD and MDA in lung tissue.…”

Helix-to-sheet transition of the Aβ42 peptide revealed using an enhanced sampling strategy and Markov state model

“…In order to clearly demonstrate the docking profile of these aggregation inhibitors, we selected a binding energy threshold of − 5 kcal/mol. This threshold was also utilized in another study [45] .

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Effects of Chinese herbal diet on hematopoiesis, immunity, and intestines of mice exposed to different doses of radiation

“…A study on the intestinal barrier function of Epimedium in piglets found that Epimedium could reduce the incidence of diarrhea, and regulate the NF-kB signaling pathway and intestinal microbiome, which effectively enhances intestinal barrier function [ 47 ]. Epimedii Folium extract could significantly attenuate cisplatin-induced intestinal damage by regulating oxidative stress, inflammation, and apoptosis, and the molecular mechanism of action might be mainly related to PI3K/Akt, p53, and NF-κB signaling pathways [ 45 ]. Achyranthes bidentata peptides play a neuroprotective role in cultured hippocampal neurons by inhibiting glutamate receptor overactivation and inhibiting Caspase-3-dependent mitochondrial apoptosis pathways [ 30 ].…”