Mechanistic Insights into Ginger’s Role in Improving Sperm Malformation Under Heat Stress Using Network Pharmacology and Molecular Docking

³ College of Biology and Food Engineering, Huaihua University, Huaihua 418000, Hunan Province, China; Key Laboratory of Research and Utilization of Ethnomedicinal Plant Resources of Hunan Province, Huaihua University, Huaihua 418000, Hunan Province, China; Hunan Provincial Higher Education Key Laboratory of Intensive Processing Research on Mountain Ecological Food, Huaihua University, Huaihua 418000, Hunan Province, China,

JCNR 2024 , 8(12), 289–294; https://doi.org/10.26689/jcnr.v8i12.9275

© 2024 by the Authors. Licensee Whioce Publishing, Singapore. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )

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Abstract

Objective: This study investigates the effects of ginger on sperm dysmorphosis under heat stress using network pharmacology and molecular docking techniques. Methods: The core components, target sites, and primary pathways of ginger were predicted using the TCMSP database. Genes associated with sperm malformation and heat stress were identified through databases such as GeneCards and DisGeNET, followed by KEGG and GO analyses based on intersections with ginger targets. Core genes identified via Cytoscape software were subjected to molecular docking with ginger’s active components. Results: The principal active components of ginger identified include β-sitosterol and dihydrocapsaicin. Network pharmacology analysis suggested that ginger exerts its effects through pathways such as the prostate cancer signaling pathway, estrogen signaling pathway, inflammatory pathways, and nuclear receptor signal transduction. These pathways may ameliorate sperm malformation symptoms caused by heat stress. Conclusion: Integrating findings from network pharmacology and molecular docking, the active components of ginger potentially modulate the expression of heat shock proteins during heat stress via inflammatory and oxidative stress pathways. This modulation may protect spermatogenesis under heat stress and improve sperm malformation.

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