Deans' stroke musings: Blood-activating, depression-relieving formula alleviates post-stroke depression: mechanistic insights from network pharmacology and microglial validation

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, July 8, 2026

Blood-activating, depression-relieving formula alleviates post-stroke depression: mechanistic insights from network pharmacology and microglial validation

You're so fucking incompetent you need to treat depression rather than having EXACT RECOVERY PROTOCOLS so that depression treatment isn't needed! I'd suggest taking up basket weaving; more in line with your IQ.

Blood-activating, depression-relieving formula alleviates post-stroke depression: mechanistic insights from network pharmacology and microglial validation

N
Na Zhao
L
Lumi Zhang
W
Wei Li
Y
Yiru Wang
Z
Zhengyu Zhu
Zhimin Wu *

Department of Neurology, Wenzhou TCM Hospital of Zhejiang Chinese Medical University, Zhejiang, China

Abstract

Introduction:

Post-stroke depression (PSD) is common and disabling, yet mechanism-based, multi-target therapies that jointly curb neuroinflammation and support cell survival are scarce. We evaluated a Blood-Activating, Depression-Relieving (BADR) herbal formula for effects on PSD-relevant molecular hubs and microglial phenotypes.

Methods:

BADR constituents from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform were standardised and mapped to human protein targets. Target-disease interaction networks were assembled in Search Tool for the Retrieval of Interacting Genes/Proteins, clustered with Molecular Complex Detection, and functionally annotated via Kyoto Encyclopedia of Genes and Genomes Orthology-Based Annotation System (KEGG/GO). For experimental validation, BV2 microglia were activated with lipopolysaccharide (LPS; 24 h) and co-treated with BADR within a pre-established non-cytotoxic range; dexamethasone (1 μM) served as comparator. Outcomes included cytokines (IL-1β, TNF-α, IL-6; enzyme-linked immunosorbent assay), expression of selected nodes (EGFR, STAT3, JUN, PIK3CA, BCL2; quantitative real-time polymerase chain reaction/western blot), viability (Cell Counting Kit-8), and apoptosis (flow cytometry).

Results:

Network analysis highlighted two dense modules enriched for PI3K-AKT, JAK–STAT, and neuroactive-ligand signaling. Hubs included EGFR, AKT1, STAT3, JUN, PIK3CA, and BCL2, with EGFR, STAT3, PIK3CA, JUN, and BCL2 prioritised for cellular validation based on topology, pathway relevance, and compound-target connectivity. In BV2 cells, BADR attenuated LPS-induced IL-1β, TNF-α, and IL-6 surges, improved viability, and reduced total apoptosis, with directionally comparable effects to dexamethasone. Mechanistically, BADR down-regulated EGFR/JUN/STAT3/PIK3CA and restored BCL2 at transcript and protein levels.

Conclusion:

By converging network-level predictions with microglial phenotyping, the formula exerts coordinated anti-inflammatory and pro-survival effects centred on the EGFR-STAT3-PI3K nodes in a PSD-relevant context. These data provide a mechanistic rationale for further phosphorylation-level and in vivo validation toward multi-target PSD therapeutics.