# The efficacy and potential pharmacological mechanism of Fufang Danshen Tablet in promoting the rehabilitation of ischemic stroke: a meta-analysis and in silico study

**Authors:** Xuan Zeng, Yichu Nie, Jierong Mo, Zhangwen Peng, Tianen Zhou, Jun Jiang

PMC · DOI: 10.3389/fneur.2026.1724630 · Frontiers in Neurology · 2026-02-12

## TL;DR

This study evaluates how well Fufang Danshen Tablet helps in recovering from ischemic stroke and explores its possible mechanism of action.

## Contribution

The study combines a meta-analysis of clinical trials with in silico methods to assess FDT's efficacy and pharmacological mechanisms in ischemic stroke.

## Key findings

- FDT combined with usual care improves neurological recovery and reduces inflammation in ischemic stroke patients.
- The AKT/GSK3β/Cyclin D1 pathway is suggested as a potential mechanism for FDT's therapeutic effects.
- FDT shows significant benefits in improving blood circulation and lipid metabolism in stroke patients.

## Abstract

Fufang Danshen Tablet (FDT) is a traditional Chinese medicine (TCM) formula with remarkable efficacy in invigorating blood and eliminating blood stasis, thus commonly used in treating ischemic stroke. However, no systemic summary has been conducted to evaluate its efficacy yet. This study aims to determine the efficacy of FDT therapy for promoting the rehabilitation of ischemic stroke and to explore the potential pharmacological mechanism through an in silico approach.

Eligible clinical trials involving FDT therapy for ischemic stroke were searched across nine online databases. Meta-analysis was conducted with RevMan and Stata software. Evaluation of the quality of evidence was performed on the GRADE system. Moreover, GEO datasets, network pharmacology, and molecular docking were employed to explore the potential pharmacological mechanism.

29 clinical trials concerning 1,634 participants were incorporated into the present meta-analysis. Compared with usual care alone, FDT combined with usual care exerted better efficacy in individuals with ischemic stroke, as evidenced by an elevated overall response rate and decreased National Institute of Health Stroke Scale (NIHSS), as well as the improvement of hemorheology, inflammation, and lipid metabolism. Moreover, meta-analysis of FDT individual intervention trials also showed significant therapeutic effects. Further network pharmacology and molecular docking analysis emphasized the potentially important role of the AKT/GSK3β/Cyclin D1 pathway for FDT to regulate oligodendrocyte precursor cells (OPCs) in treating ischemic stroke.

FDT appears to significantly enhance neurological recovery, promote blood circulation, inhibit the inflammatory cascade, and lower blood lipid levels in patients with ischemic stroke. The AKT/GSK3β/Cyclin D1 pathway was predicted to be a potential mechanism of FDT in intervening ischemic stroke. In the future, more long-term follow-up RCTs with high quality are urgently needed, as well as experimental validations for the pharmacological mechanism.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420251015475, CRD420251015475.

## Linked entities

- **Proteins:** AKT1 (AKT serine/threonine kinase 1), GSK3B (glycogen synthase kinase 3 beta), ccnd1.S (cyclin D1 S homeolog)
- **Diseases:** ischemic stroke (MONDO:1060198)

## Full-text entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SIRT2 (sirtuin 2) [NCBI Gene 22933] {aka SIR2, SIR2L, SIR2L2}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, COG2 (component of oligomeric golgi complex 2) [NCBI Gene 22796] {aka CDG2Q, LDLC}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, GSK3B (glycogen synthase kinase 3 beta) [NCBI Gene 2932], CCND1 (cyclin D1) [NCBI Gene 595] {aka BCL1, D11S287E, PRAD1, U21B31}, CDK5 (cyclin dependent kinase 5) [NCBI Gene 1020] {aka LIS7, PSSALRE}
- **Diseases:** Inflammation (MESH:D007249), epilepsy (MESH:D004827), Hyperlipidemia (MESH:D006949), cerebral damages (MESH:D002539), thrombosis (MESH:D013927), brain tissue injuries (MESH:D001930), demyelination (MESH:D003711), pain (MESH:D010146), blood supply disorder (MESH:D006402), NIHSS (MESH:C538175), death (MESH:D003643), atherosclerotic (MESH:D050197), OGD (MESH:C536050), cardiovascular and cerebrovascular diseases (MESH:D002318), cerebral tissue ischemia (MESH:D002545), brain infarction (MESH:D020520), Ischemic stroke (MESH:D002544), cerebrovascular disease (MESH:D002561), hemorrhagic stroke (MESH:D000083302), neuroinflammation (MESH:D000090862), axonal degeneration (MESH:D009410), infarction (MESH:D007238), OPC injury (MESH:C564935), dementia (MESH:D003704), Stroke (MESH:D020521), Neurological Deficit (MESH:D009461), necrosis (MESH:D009336), cognitive impairment (MESH:D003072), hypoxia (MESH:D000860), motor dysfunction (MESH:D000068079)
- **Chemicals:** F1 (-), dihydrotanshinone I (MESH:C000713095), oxygen (MESH:D010100), cryptotanshinone (MESH:C037886), protocatechuic aldehyde (MESH:C005581), protopanaxadiol (MESH:C062916), ginsenoside Rg1 (MESH:C035054), TG (MESH:D014280), ginsenoside Rk3 (MESH:C472075), Tanshinone IIA (MESH:C021751), lipid (MESH:D008055), glucose (MESH:D005947), cholesterol (MESH:D002784)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Panax notoginseng (notoginseng, species) [taxon 44586]

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## References

75 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935622/full.md

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Source: https://tomesphere.com/paper/PMC12935622