Praveen Deepak

Magadh University
India

Abstract Title:

Biography:

Praveen Deepak Assistant Professor, Department of Zoology, Magadh University, Bodhgaya, India Praveen Deepak is an Assistant Professor of Zoology at Magadh University, Bodhgaya, India. His research focuses on Cancer Immunology and Experimental Therapeutics for Rheumatoid Arthritis, with a particular interest in the therapeutic potential of natural products. He has previously worked at Banaras Hindu University (BHU), Varanasi, India, as a Junior and Senior Research Fellow, studying immune modulation in tumour models. He continues to pursue translational research in immunopathophysiology and mentors students in the field.

Research Interest:

Title: Targeting STAT3 Signalling in Rheumatoid Arthritis: Computational Evidence for Epigallocatechin as a Natural Modulator

Complementary and alternative medicine increasingly contributes to the management of chronic inflammatory disorders through the use of naturally derived bioactive compounds with immunomodulatory potential. Rheumatoid arthritis (RA) is a systemic autoimmune disease characterised by persistent synovial inflammation, aberrant immune activation, and progressive joint damage, for which current therapeutic strategies remain limited by adverse effects and incomplete efficacy. Signal Transducer and Activator of Transcription 3 (STAT3) is a central mediator of pro-inflammatory signalling and immune persistence in RA, rendering it a compelling molecular target. Epigallocatechin (EGC), a predominant green tea polyphenol widely employed in complementary therapeutic practices, has demonstrated anti-inflammatory activity; however, its molecular interactions with STAT3 are not fully defined. In this study, a comprehensive in silico approach was applied to elucidate the mechanistic basis of EGC-mediated STAT3 modulation. Molecular docking, molecular dynamics simulations, and binding free energy analyses were conducted to evaluate binding affinity, conformational stability, and residue-specific interactions. The results indicate a stable association of EGC with functionally critical regions of STAT3, suggesting potential interference with its activation and dimerisation processes. Pathway-level interrogation further implicates suppression of STAT3-dependent inflammatory signalling relevant to RA pathophysiology. Collectively, these findings provide mechanistic computational support for epigallocatechin as a natural STAT3 modulator and highlight the translational relevance of in silico methodologies in advancing evidence-based complementary therapeutic strategies for rheumatoid arthritis.