Efficacy and Molecular Mechanism of Epigallocatechin-3-gallate in Spinal Cord Injury: A Meta-analysis, Network Pharmacology Analysis, and Molecular Docking Study.

Authors

Jia-Xin Wen, Ai-Fang Zhou, Yu Xiao, Shi-Pian Li, Hao-Wen Lin, Yue-Li Sun, Bi-Meng Zhang, Yong-Jun Wang, Xue-Jun Cui, Yun-Zhao Gong, Min Yao

Published in

Current neuropharmacology. Sep 30, 2026. Epub Sep 30, 2026.

Abstract

Spinal Cord Injury (SCI) remains a major clinical challenge because of limited therapeutic options and poor prognosis. Epigallocatechin-3-gallate (EGCG) can cross the blood-brain barrier and has demonstrated neuroprotective properties. However, its therapeutic efficacy and underlying mechanisms in SCI remain incompletely understood.
A comprehensive literature search was conducted in PubMed, ScienceDirect, Web of Science, the China National Knowledge Infrastructure, and Wanfang databases through August 2025 to identify studies evaluating the effects of EGCG in animal models of SCI. Meta-analyses and subgroup analyses were performed using Review Manager version 5.3. Network pharmacology was used to identify potential therapeutic targets and signaling pathways, followed by molecular docking and Molecular Dynamics (MD) simulations to evaluate the interactions between EGCG and core targets.
A total of 22 studies were included. Pooled analyses showed that EGCG significantly improved motor function in animals with SCI, as demonstrated by higher Basso, Beattie, and Bresnahan (BBB) scores on day 28 (9 studies, n = 139/99, WMD = 3.96 (2.79, 5.13), p < 0.00001) and higher inclined plane test scores (3 studies, n = 59/37, WMD = 13.14 (12.48, 13.79), p < 0.00001). Subgroup analyses indicated greater improvements following intrathecal administration (4 comparisons from 2 studies, (27, 28), n = 44/22, WMD = 2.95 (2.03, 3.88), p < 0.00001) and in female animals (8 comparisons from 4 studies (24, 27, 28, 30), n = 74/41, WMD = 2.40 (1.82, 2.97), p < 0.00001). EGCG also significantly reduced lipid peroxidation and inflammatory responses and exerted anti-apoptotic effects (MDA: 14 comparisons from 7 studies (22-24, 34, 35, 37, 38), n = 93/49, SMD = -3.18 (-3.88, -2.48), p < 0.00001; iNOS: 7 comparisons from 3 studies (22, 25, 35), n = 44/19, SMD = -3.19 (-4.12, -2.25), p < 0.00001; Bcl-2: 13 comparisons from 6 studies (24, 27, 28, 35, 37, 43), n = 75/35, SMD = 3.61 (2.64, 4.58), p < 0.00001). Network pharmacology analysis identified the MAPK and PI3K-AKT signaling pathways as key pathways potentially underlying the therapeutic effects of EGCG in SCI. Molecular docking and MD simulations further supported stable interactions between EGCG and the core targets AKT1 and MMP9.
The integrated findings suggest that EGCG exerts neuroprotective effects through coordinated regulation of oxidative stress, inflammation, apoptosis, autophagy, astrocyte function, and angiogenesis via multiple interconnected signaling pathways. Subgroup analyses further suggested greater therapeutic efficacy in female animals and following intrathecal administration, although the biological mechanisms underlying these differences require further investigation.
EGCG demonstrates therapeutic potential in experimental SCI by promoting neurological recovery through the coordinated modulation of multiple pathological processes. By integrating meta-analysis with network pharmacology, molecular docking, and MD simulations, this study provides preclinical evidence and mechanistic support for further investigation of EGCG as a candidate treatment for SCI. Additional well-designed preclinical and clinical studies are required to confirm its efficacy, safety, and translational potential.

PMID:
42852775
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.

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