| Aspirin / ASA |
NSAID / antiplatelet drug |
Irreversible COX-1 inhibition; ↓ thromboxane A2;
↓ platelet aggregation
|
Reduces recurrent ischemic stroke risk in appropriate
non-cardioembolic ischemic stroke patients
|
Strong clinical; standard of care
|
Acute after hemorrhage is excluded + secondary prevention
|
Common long-term antiplatelet dose: approximately 75–100 mg/day;
higher doses may be used in specific clinical circumstances
|
High; established benefit, but bleeding-risk limited
|
| N-Acetylcysteine (NAC) |
Thiol antioxidant / glutathione precursor |
↑ glutathione; ↓ ROS; ↓ lipid peroxidation;
anti-inflammatory effects; thiol/disulfide modulation;
possible reduction of large VWF multimers
|
Preliminary human evidence for improved neurological and functional
recovery; reduction of oxidative and inflammatory biomarkers;
possible antithrombotic/VWF effects
|
Randomized human pilot studies + strong preclinical evidence
|
Acute / early recovery
|
No established routine post-stroke supplement dose.
One clinical study used a 4 g loading dose followed by
4 g/day divided for 2 days; this is a research protocol,
not a routine self-treatment dose
|
Moderate–High; promising human evidence but not standard therapy
|
| Melatonin |
Indoleamine / neurohormone |
↓ ROS; mitochondrial protection; ↓ neuroinflammation;
↓ apoptosis; ↓ excitotoxicity; BBB protection;
possible ↓ MMP-9 and NLRP3 signaling
|
Reduced ischemia-reperfusion injury in experimental models;
preliminary human evidence suggests improved neurological
and functional recovery
|
Preliminary randomized clinical + extensive preclinical evidence
|
Acute + recovery; sleep/circadian support
|
No established stroke-treatment dose.
Low-dose sleep supplementation is commonly approximately
0.3–2 mg at night, while stroke trials have used
study-specific pharmacological protocols
|
Moderate–High; favorable safety profile at conventional doses,
promising but unproven stroke efficacy
|
| Vitamin D3 |
Vitamin / secosteroid hormone precursor |
Immune modulation; neurotrophic support; muscle function;
vascular/endothelial support; calcium homeostasis
|
May improve neurological and functional rehabilitation outcomes,
particularly in vitamin-D-deficient patients
|
Clinical studies + systematic review/meta-analysis; mixed but positive signal
|
Recovery / deficiency correction
|
Dose should be based on serum 25-OH-vitamin D status;
no universal stroke-specific dose
|
Moderate–High when deficient
|
| Hydrogen Gas / Molecular Hydrogen |
Therapeutic medical gas |
↓ ischemia/reperfusion oxidative stress; ↓ neuroinflammation; mitochondrial protection; ↓ apoptosis; BBB protection |
Potential reduction of secondary neuronal injury and improvement in early neurological recovery |
Small human RCT + substantial preclinical evidence |
Primarily acute / early recovery |
Clinical stroke study: 3% H₂ inhalation, 1 h twice daily for 7 days |
Promising but experimental; chronic rehabilitation benefit unproven |
| Coenzyme Q10 / CoQ10 |
Mitochondrial cofactor / antioxidant |
Supports mitochondrial electron transport;
↓ ROS; ↑ antioxidant capacity;
anti-inflammatory effects
|
Human studies suggest reductions in oxidative stress and inflammatory
biomarkers after ischemic stroke; possible neurological benefit
|
Small randomized human trials + preclinical evidence
|
Acute + recovery
|
Study-specific; no established post-stroke therapeutic dose.
Common supplement doses are approximately 100–300 mg/day
|
Moderate; encouraging human evidence but not standard therapy
|
| Ginkgo biloba / EGb 761 |
Standardized herbal extract |
Cerebral microcirculation; antioxidant effects;
platelet-activating-factor modulation; neuroprotection
|
May support post-stroke cognition and neurological recovery;
not established for prevention of recurrent stroke
|
Clinical + preclinical; evidence stronger for standardized EGb 761
|
Recovery / cognition
|
Approximately 120–240 mg/day standardized extract
in many neurological studies
|
Moderate; bleeding interaction caution, especially with
antiplatelet or anticoagulant drugs
|
| Panax notoginseng / PNS |
Triterpene saponins |
Anti-inflammatory; vascular/endothelial protection;
microcirculation support; antiplatelet/antithrombotic effects;
antioxidant activity
|
Improved neurological and blood-flow outcomes in some clinical studies;
much evidence involves standardized PNS or Xuesaitong preparations
|
Clinical mainly from China + substantial preclinical evidence
|
Acute + recovery
|
Highly formulation-dependent; standardized extracts and injectable
preparations cannot be directly equated with ordinary root supplements
|
Moderate; possible bleeding interaction
|
| Alpha-GPC / Alpha-glycerylphosphorylcholine |
Choline donor / phospholipid precursor |
↑ acetylcholine; phosphatidylcholine synthesis;
neuronal membrane support
|
May support cognitive and neurological recovery after stroke
|
Older human clinical evidence; modern confirmation limited
|
Recovery / cognition
|
Approximately 300–1200 mg/day in supplement/clinical use;
no established modern stroke-treatment dose
|
Moderate; possible TMAO/cardiovascular concern remains uncertain
|
| Citicoline / CDP-choline |
Choline donor / phospholipid precursor |
↑ phosphatidylcholine synthesis; membrane repair;
↓ free fatty acid release; cholinergic support
|
Strong mechanistic rationale and possible cognitive effects,
but no demonstrated benefit in the large ICTUS acute-stroke trial
|
Clinical; large pivotal RCT negative, smaller/earlier studies mixed
|
Recovery / cognition
|
Approximately 500–2000 mg/day has been studied;
no established effective post-stroke dose
|
Low–Moderate efficacy / good tolerability
|
| Salvia miltiorrhiza / Danshen |
Herbal extract |
Microcirculation; endothelial protection;
antioxidant effects; antiplatelet activity
|
May support cerebral perfusion and neurological recovery;
evidence often involves Chinese standardized or injectable preparations
|
Clinical mainly China + preclinical
|
Acute + recovery
|
Variable and formulation-dependent;
no established dose for ordinary oral supplements after stroke
|
Moderate; bleeding and drug-interaction caution
|
| Vitamin B12 + Folate + Vitamin B6 |
B vitamins / methylation cofactors |
↓ homocysteine; methylation support;
endothelial and neurological function
|
Potential secondary-prevention relevance when homocysteine is elevated
or B12/folate deficiency is present
|
Human clinical; mixed overall, stronger rationale in selected patients
|
Prevention / recovery / deficiency correction
|
Dose should be guided by B12, folate, renal function,
and homocysteine status
|
Moderate when indicated
|
| Magnesium |
Essential mineral |
NMDA modulation; vascular tone; blood-pressure regulation;
neuronal membrane stabilization
|
Supports normal vascular and neurological function;
direct therapeutic benefit after established stroke remains uncertain
|
Nutritional/epidemiological support; limited treatment evidence
|
Prevention / recovery / deficiency correction
|
Prefer dietary adequacy and correction of deficiency;
no established post-stroke therapeutic supplement dose
|
Moderate when deficient
|
| Omega-3 / EPA / DHA |
Marine fatty acids |
Lipid modulation; endothelial effects;
inflammation modulation; membrane support
|
Cardiovascular risk-factor support, but ordinary fish-oil
supplementation has not consistently reduced recurrent stroke
|
Human clinical; mixed for stroke-specific outcomes
|
Prevention / long-term vascular health
|
Prefer dietary fish intake; supplemental dose should be individualized,
especially when combined with antithrombotic drugs
|
Moderate for cardiovascular support; Low–Moderate for stroke-specific benefit
|
| Baicalin |
Flavonoid |
Anti-inflammatory; anti-apoptotic;
antioxidant; PI3K/Akt and related signaling
|
Reduced neuronal injury, inflammation, and infarct size
in experimental ischemia models
|
Preclinical + limited clinical context
|
Experimental acute neuroprotection
|
No established human stroke dose
|
Low–Moderate
|
| Curcumin |
Polyphenol |
↓ NF-κB; ↓ inflammatory cytokines;
Nrf2 activation; antioxidant and anti-apoptotic effects
|
Reduced infarct size, oxidative stress, and neuroinflammation
in experimental ischemia models
|
Strong preclinical; limited direct human stroke evidence
|
Experimental acute + recovery
|
General supplement doses commonly approximately 500–2000 mg/day
depending on formulation; no established stroke dose
|
Low–Moderate; bioavailability and bleeding-interaction considerations
|
| Resveratrol |
Polyphenol |
SIRT1 activation; mitochondrial protection;
antioxidant; anti-inflammatory; anti-apoptotic
|
Reduced apoptosis and ischemic brain injury in experimental models
|
Strong preclinical; limited direct clinical stroke evidence
|
Experimental acute + recovery
|
General supplement doses approximately 100–500 mg/day;
no established stroke-treatment dose
|
Low–Moderate; low bioavailability
|
| EGCG |
Green-tea catechin |
ROS modulation; Nrf2-related antioxidant activity;
vascular and mitochondrial protection
|
Reduced neuronal injury and oxidative stress in experimental models
|
Strong preclinical; little direct human stroke evidence
|
Experimental acute neuroprotection
|
Approximately 200–400 mg/day supplemental EGCG is commonly used;
no established stroke dose
|
Low–Moderate; hepatotoxicity risk increases with high-dose extracts
|
| Quercetin |
Flavonoid |
Antioxidant; anti-inflammatory;
anti-edema; endothelial protection
|
Reduced edema, oxidative injury, and infarct size
in experimental ischemia models
|
Strong preclinical; limited direct clinical stroke evidence
|
Experimental acute neuroprotection
|
Approximately 500–1000 mg/day commonly used as a supplement;
no established stroke dose
|
Low–Moderate
|
| Tocotrienols |
Vitamin E subfamily |
Lipid antioxidant; membrane protection;
anti-inflammatory and neuroprotective signaling
|
Neuroprotection and reduced ischemic injury in experimental models
|
Preclinical + limited human neurological evidence
|
Experimental acute / prevention
|
Approximately 100–300 mg/day commonly used in supplements;
no established stroke dose
|
Low–Moderate
|
| Luteolin |
Flavonoid |
↓ NF-κB; Nrf2 activation;
PI3K/Akt modulation; anti-inflammatory;
anti-apoptotic effects
|
Reduced inflammation and neuronal injury in experimental stroke models
|
Strong preclinical
|
Experimental acute neuroprotection
|
No established human stroke dose
|
Low
|
| Ferulic acid |
Phenolic acid |
Antioxidant; vasodilation;
endothelial and vascular protection
|
Improved cerebral blood flow and reduced neuronal injury
in experimental models
|
Preclinical
|
Experimental acute neuroprotection
|
No established human stroke dose
|
Low
|
| Rosmarinic acid |
Phenolic acid |
BBB protection; antioxidant;
anti-inflammatory; anti-apoptotic
|
Reduced BBB disruption, edema, and inflammatory injury
in experimental ischemia models
|
Preclinical
|
Experimental acute neuroprotection
|
No established human stroke dose
|
Low
|
| Berberine |
Isoquinoline alkaloid |
AMPK activation; metabolic regulation;
anti-inflammatory, antioxidant, and endothelial effects
|
Neuroprotection in experimental ischemia;
may also improve metabolic vascular risk factors
|
Predominantly preclinical for stroke
|
Prevention + experimental recovery
|
Approximately 500–1500 mg/day commonly used metabolically;
no established stroke-treatment dose
|
Low–Moderate; substantial drug-interaction potential
|
| Huperzine A |
Alkaloid / acetylcholinesterase inhibitor |
AChE inhibition; ↑ acetylcholine;
possible NMDA modulation and neuroprotection
|
Potential support for post-stroke cognitive dysfunction,
but direct clinical evidence is limited
|
Preclinical + indirect cognitive clinical evidence
|
Experimental recovery / cognition
|
Approximately 100–200 µg/day commonly used;
no established stroke-treatment dose
|
Low; cholinergic adverse effects may limit use
|
| Honokiol |
Biphenolic lignan |
Mitochondrial protection; antioxidant;
anti-inflammatory; anti-apoptotic effects
|
Reduced ischemic neuronal injury in experimental models
|
Preclinical
|
Experimental acute + recovery
|
No established human stroke dose
|
Low
|