Research Journal of Pharmacognosy (Jul 2025)
Unraveling the Immune Modulating Potential of Zingiber officinale Bioactive Compounds in Infants Born to Obese Mothers: a Network Pharmacology Approach
Abstract
Background and objectives: Pregnant mothers with obesity may increase the risk of adverse health outcomes for their infants, such as weakened immune systems. Currently, there is no standardized treatment for obese pregnant women to reduce risks to the mothers and their infants. Zingiber officinale (ginger) is a commonly used medicinal plant to relieve symptoms associated with hyperemesis gravidarum. The bioactive compounds in ginger are recognized for their anti-obesity and anti-inflammatory properties. Our objective was to investigate how the phytochemical components of ginger may interact with immune response proteins related to infants of obese mothers, employing a network pharmacology approach. Method: The target proteins were obtained from Gene Cards, and the chemical structures were sourced from PubChem. Protein-protein interactions were constructed using Cytoscape. Interactions between phytochemicals from ginger and target genes were illustrated, followed by enrichment analysis and molecular docking. Results: Through network pharmacology and molecular docking, we identified 36 bioactive compounds in Zingiber officinale that modulate key proteins (TLR4, NF-κB, TNF-α) involved in inflammation and cytokine production. The main phytoconstituents, 6-gingerol, and 6-shogaol, demonstrated strong binding affinity to TLR4, as revealed by the docking analysis, identifying them as ligands that bind effectively to the target protein TLR4. This finding is significant, given TLR4's role in addressing obesity-related developmental inflammation. Conclusion: This study emphasizes the immunomodulatory potential of bioactive compounds from Zingiber officinale, particularly 6-gingerol and 6-shogaol, in addressing immune system dysregulation associated with obesity in children born to obese mothers, focusing on key targets such as TLR4, NF-κB, and TNF-α.
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