Vitamin C exerts anti-cadmium induced fracture functions/targets: bioinformatic and biostructural findings

Background: Epidemiological data indicate an association between cadmium exposure and risk of bone fracture; however, clinical treatment of cadmium-induced fracture is limited. Although vitamin C (VC) reportedly reduces cadmium-induced fracture, its pharmacological mechanism remains unexplored. Methods: Thus, we used a network pharmacology approach and molecular docking analysis to identify core targets, functional processes, and biological pathways involved in the anti-fracture action of VC. Results: Bioinformatics identified 17 intersection targets of VC and cadmium-induced fracture. Nine core targets were characterized, including tumor protein p53, epidermal growth factor receptor, proto-oncogene c, mitogen-activated protein kinase-1 (MAPK1), MAPK3, signal transducer and activator of transcription-3, MAPK14, prostaglandin-endoperoxide synthase 2, and estrogen receptor alpha. Interestingly, findings of molecular docking analysis indicated that VC exerted effective binding capacity in cadmium-induced fracture. Furthermore, biological processes, cell components, molecular functions, and pharmacological pathways involved in the action of VC against cadmium-induced fracture were identified and visualized. Conclusions: Based on these findings, we conclude that VC exhibits its anti-cadmium-induced fracture effects by promoting osteoblastic regeneration and proliferation, and inhibiting inflammatory stress. The core targets may serve as biomarkers for diagnosing cadmium-induced fractures. (c) 2022 Beijing Academy of Food Sciences. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Automated summary

Using a network pharmacology approach and molecular docking analysis, this study explores the pharmacological mechanism of vitamin C (VC) in reducing cadmium-induced fracture. The study identifies 17 intersection targets of VC and cadmium-induced fracture, and reveals that VC exerts effective binding capacity in cadmium-induced fracture. Furthermore, the study identifies the biological processes, cell components, molecular functions, and pharmacological pathways involved in the action of VC against cadmium-induced fracture.