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image of Exploring the Potential of Nuciferine in Diabetes Management via PTGS2 Pathway Targeting by Network Analysis and in-silico Modeling Approach

Abstract

Introduction

Diabetes mellitus, a chronic metabolic disorder characterized by elevated blood glucose levels, has emerged as a significant global health burden. Chronic inflammation and insulin resistance are central to the pathogenesis of non-insulin-dependent (type 2) diabetes mellitus. PTGS2 (prostaglandin-endoperoxide synthase 2) has been implicated in inflammatory pathways associated with diabetic complications, making it a potential therapeutic target.

Methods

Advanced computational methodologies were employed to identify potential natural compounds with anti-diabetic activity. Techniques included network pharmacology to establish compound-target-pathway relationships and molecular docking to evaluate binding affinity and interaction profiles of selected phytochemicals with PTGS2.

Results

PTGS2 and its downstream prostaglandin pathways were strongly associated with diabetic inflammation and insulin resistance. Molecular docking identified Corytuberine and Nuciferine as having high binding affinities with PTGS2. Network pharmacology analysis confirmed Nuciferine’s connection to PTGS2, supporting its role as a bioactive agent targeting diabetes-related inflammatory processes.

Discussion

The findings suggest that PTGS2 contributes to the progression of insulin resistance and chronic inflammation in type 2 diabetes. Targeting this enzyme with bioactive compounds such as Nuciferine may offer therapeutic benefits. However, translational studies and clinical trials are essential to validate these computational predictions and assess safety and efficacy .

Conclusion

Nuciferine exhibits promising potential in modulating PTGS2 activity and improving insulin sensitivity. Continued research and clinical validation are needed to confirm its efficacy and support the development of novel anti-diabetic therapies targeting inflammatory pathways.

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2025-09-26
2025-11-05
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