Apigenin is a plant-derived flavonoid found in chamomile, parsley, celery, and several other common foods. Beyond its well-studied effects on sleep and anxiety, apigenin has attracted research attention for potential cardiovascular benefits, particularly around blood pressure regulation and the health of blood vessel linings. These are meaningful targets: endothelial dysfunction is considered an early, modifiable step in cardiovascular disease progression.
The research on apigenin and cardiovascular function is real but still developing. Most studies have been conducted in cell cultures or animal models, and large human clinical trials are limited. This article walks through what the current evidence shows, explains the proposed biological mechanisms in plain terms, and is honest about where the science is strong versus where significant gaps remain. These statements have not been evaluated by the FDA; apigenin is not intended to diagnose, treat, cure, or prevent any disease.
Key Takeaways
- In cultured endothelial cells, apigenin increased nitric oxide production through calcium and PI3-kinase/Akt signaling [1], and in isolated arteries from hypertensive rats it relaxed vessels partly through nitric oxide[2]. Whether this lowers blood pressure in people has not been shown [1][2].
- In old mice given apigenin in their drinking water, apigenin reversed aortic stiffening [3], reduced oxidative stress, and lowered vascular inflammation: three interconnected aspects of cardiovascular aging [3].
- Apigenin belongs to a class of flavonoids with recognized antihypertensive activity in experimental models, but human clinical trial data remains limited [4][5].
- Celery and chamomile are practical dietary sources; in lab studies apigenin inhibited CYP1A2, CYP2C9, and CYP3A4, which could in theory affect warfarin, statins, and other medications metabolized by them, though these are enzyme-assay results, not demonstrated interactions in people [13][14][15][16][17].
- The research is genuinely interesting but should not be interpreted as proof that apigenin supplements treat or prevent cardiovascular disease in humans.
Why Blood Vessels Matter: A Brief Primer on Endothelial Function
The endothelium is the thin layer of cells lining every blood vessel in your body. It does far more than serve as a passive barrier: it actively regulates vascular tone, inflammation, platelet aggregation, and blood flow by releasing signaling molecules, most notably nitric oxide (NO). When endothelial function is impaired, vessels lose their ability to dilate appropriately, and chronic low-grade vascular inflammation can set in. This state, called endothelial dysfunction, is an early marker of cardiovascular risk and a contributing factor to elevated blood pressure.
Dietary polyphenols, including flavonoids like apigenin, have been studied as potential modulators of endothelial health. A 2015 review noted that dietary polyphenols can regulate endothelial function through multiple pathways, with nitric oxide bioavailability as a central mechanism [6]. Apigenin sits within this broader class of compounds, but it has several pharmacological properties that distinguish it from other flavonoids.
Apigenin and Nitric Oxide: The Vasodilation Pathway
Nitric oxide is produced by an enzyme called endothelial nitric oxide synthase (eNOS). When eNOS is activated, it generates NO, which diffuses into smooth muscle cells lining blood vessels and triggers relaxation: reducing vascular resistance and, in turn, blood pressure. Research has shown that apigenin can activate eNOS through calcium-dependent and phosphatidylinositol 3-kinase/Akt-dependent signaling pathways, leading to increased nitric oxide production in endothelial cells [1].
Research note: In mice given the chemotherapy drug Adriamycin, oral apigenin protected against cardiotoxicity markers and cardiomyocyte apoptosis, via the PI3K/AKT/mTOR pathway; mouse result only [25].
Earlier work confirmed that flavonoids as a class can stimulate nitric oxide synthase activity [7], and apigenin specifically has been examined in the context of resistance vessels: the small arteries most responsible for peripheral vascular resistance and blood pressure control. A 2024 study in isolated mesenteric vessels from hypertensive rats found that apigenin relaxed the vessels, partly through nitric oxide and calcium-activated potassium channel mechanisms [2], suggesting the effect involves more than one complementary pathway [2].
It is worth noting that some of the estrogen-like signaling observed with certain polyphenols may also play a role in eNOS activation. Research on wine-derived polyphenols showed estrogen receptor-mediated nitric oxide synthesis in human endothelial cells [8], a mechanism that has not been shown for apigenin itself, so its practical significance in humans at typical dietary intakes remains uncertain.
Reversing Endothelial Aging: Evidence from Animal Studies
One of the more compelling preclinical studies on apigenin and vascular health examined aged mice given apigenin supplementation. The researchers found that apigenin restored endothelial function by reducing oxidative stress, reversed aortic stiffening (a key measure of large-artery aging), and reduced markers of vascular inflammation [3]. These are three distinct but interrelated aspects of cardiovascular aging, and the fact that a single compound appeared to address all three in the same model is noteworthy.
In old mice, apigenin in drinking water restored artery dilation and eased aortic stiffening
Mice, 6 weeks
Old mice (27 months) drank apigenin at 0.5 mg/mL in their drinking water for 6 weeks. Young mice (6 months) were the comparison.
Restored to 96%
Carotid artery endothelium-dependent dilation in old mice was restored to 96%, near the young-mouse level, by increasing nitric oxide availability.
Pulse wave velocity 373 cm/s
Age-associated aortic stiffening was mitigated. Pulse wave velocity in treated old mice was 373 cm/s; the untreated value is not shown here.
In old mice, apigenin improved artery function, and that has not been shown in people.
Male C57BL/6N mice, young and old. Animal data from one study. Source: Clayton et al., American journal of physiology. Heart and circulatory physiology 2021
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Aortic stiffness is clinically significant because it increases the workload on the heart and is independently associated with cardiovascular events. Oxidative stress damages the endothelium by reducing NO bioavailability: reactive oxygen species can quench nitric oxide before it reaches smooth muscle cells. Apigenin’s antioxidant capacity may therefore support NO signaling indirectly, in addition to its direct eNOS-activating effects [3].
These findings are promising but must be interpreted with caution. Animal models of vascular aging do not always translate directly to human outcomes. The doses used in animal studies are frequently higher than what a typical supplement provides, and the mechanistic pathways, while plausible, have not been confirmed in large human trials.
Flavonoids and Blood Pressure: Where Apigenin Fits
Apigenin does not exist in isolation: it belongs to a well-studied family of plant compounds with a recognized track record in hypertension research. A 2024 review of flavonoids and hypertension described multiple mechanisms through which this class of compounds may lower blood pressure, including ACE inhibition, calcium channel modulation, eNOS activation, and antioxidant effects [4]. Another review focused specifically on flavonoids from Chinese herbal medicine documented apigenin among the compounds with antihypertensive potential [9].
Celery is one of the richest dietary sources of apigenin, and a 2024 narrative review on celery’s antihypertensive properties highlighted its flavonoid content as a likely contributor to blood pressure effects observed in animal models [10]. A broader phytotherapy review similarly noted that plants rich in flavonoids like apigenin show antihypertensive activity in experimental settings [11].
A review of flavonoid effects in animal models of hypertension found evidence across multiple experimental paradigms for blood-pressure-lowering activity in this compound class [5]. Again, the consistent theme is promising preclinical data paired with a recognized need for more human clinical evidence before confident conclusions can be drawn.
Mitochondrial Health and Vascular Function: An Emerging Link
A newer area of cardiovascular research focuses on mitochondrial dysfunction as a driver of hypertension. Vascular smooth muscle cells and endothelial cells are energy-intensive and depend on healthy mitochondria for normal function. When mitochondrial efficiency declines, reactive oxygen species production increases, endothelial NO signaling is impaired, and vascular inflammation worsens. A 2026 mechanistic review described these mitochondrial pathways as therapeutically relevant targets in hypertension [12].
Whether apigenin affects mitochondrial function in ways that matter for blood pressure is a hypothesis, not an established finding. However, the direct connection between apigenin’s mitochondrial activity and clinical blood pressure outcomes in humans has not been established. This remains a hypothesis worth watching as research matures.
Practical Considerations: Dietary Sources and Supplement Context
Apigenin is present in chamomile tea, parsley, celery, and to a lesser extent in many other fruits and vegetables. Chamomile tea is one of the most convenient and widely consumed sources. Supplemental apigenin is also available, typically in capsule form at doses ranging from 50 mg to 500 mg per day, though no established therapeutic dose has been confirmed for cardiovascular endpoints in human trials.
Anyone considering apigenin supplementation for cardiovascular reasons should be aware of several drug interactions. In lab studies, apigenin inhibited cytochrome P450 enzymes CYP1A2, CYP2C9, and CYP3A4. In theory this could alter the metabolism of medications processed by these pathways [13][14][15][16][17]including warfarin, certain statins, and some calcium channel blockers. Individuals taking blood pressure medications, anticoagulants, or other cardiovascular drugs should consult their prescribing physician before adding apigenin supplements. Apigenin has been linked to sedation in some animal and cell work, but the findings conflict: in cell studies it inhibited GABA-A receptors rather than boosting them and did not act through the benzodiazepine site. Stacking with other sedatives, alcohol, or benzodiazepines is a theoretical concern that warrants caution [18][19][20][21].
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As an Amazon Associate we earn from qualifying purchases. Apigenin products differ mainly in what else is in the capsule (some are plain apigenin, others blend it with L-theanine, valerian root or magnesium) so check the label for the actual apigenin dose per serving, and prefer products that publish third-party testing.
A Note on the Evidence
Most evidence for apigenin’s cardiovascular effects comes from cell and animal studies; human clinical trial data is limited, so claims about blood pressure benefits in people should be understood as preliminary. In lab studies apigenin inhibited CYP1A2, CYP2C9, and CYP3A4, which could in theory interact with warfarin, statins, calcium channel blockers, and benzodiazepines [13][14][15][16][17]individuals on any prescription cardiovascular or anticoagulant medication should consult their physician before use. These statements have not been evaluated by the FDA; apigenin is not intended to diagnose, treat, cure, or prevent any disease.
Apigenin and Blood Pressure: The Short Version
Apigenin has shown blood-pressure-relevant effects on endothelial function in cell and animal research, largely through mechanisms tied to vascular relaxation. Large human clinical trials specifically on apigenin and blood pressure are still limited, so this is an early, biologically plausible area rather than an established clinical effect. See the full research breakdown above for the specific studies and their limitations.
Frequently Asked Questions
How does apigenin affect blood pressure mechanistically?
Apigenin appears to work through several pathways simultaneously. It activates eNOS via calcium and PI3K/Akt signaling to increase nitric oxide production, which relaxes vascular smooth muscle [1]. It also activates calcium-sensitive potassium channels in resistance vessels, contributing to vasodilation in hypertensive animal models [2]. Antioxidant activity may further protect nitric oxide from degradation by reactive oxygen species.
The human blood pressure findings that do exist come from chamomile, not apigenin. In a chamomile extract anxiety trial, mean arterial blood pressure was lower than with placebo as a secondary finding (P = 0.0063), and inhaling chamomile essential oil lowered blood pressure in 154 patients with acute coronary syndrome. Neither result isolates apigenin [23][24].
Is there human clinical trial evidence for apigenin and blood pressure?
Current evidence is predominantly from cell culture and animal studies. Reviews of flavonoids and hypertension identify apigenin as a promising compound with mechanistic support [4][9], but large, well-controlled human randomized trials specifically testing apigenin for blood pressure are lacking. Dietary celery, a rich source of apigenin, has been reviewed for antihypertensive effects [10], but isolating apigenin’s contribution from other compounds in whole foods is difficult.
What does 'endothelial function' mean and why does it matter for heart health?
The endothelium is the inner lining of blood vessels. When healthy, it regulates vascular tone, prevents clotting, and controls inflammation through nitric oxide and other signals. When impaired, vessels become rigid and inflamed, increasing blood pressure and cardiovascular risk. Dietary polyphenols including flavonoids like apigenin have been studied for their ability to support endothelial function [6], with one study specifically showing apigenin restored endothelial function and reversed aortic stiffness in aged mice [3].
Can I get enough apigenin from food, or do I need a supplement?
Chamomile tea, parsley, and celery are meaningful dietary sources of apigenin. Whether dietary intake is sufficient to replicate the effects seen in animal studies, where doses are often higher and more controlled, is unknown. Supplemental apigenin provides more predictable amounts, but no established cardiovascular dose has been validated in human trials. For most people, increasing intake of apigenin-rich foods is a reasonable, lower-risk starting point.
Does apigenin interact with blood pressure medications?
Possibly, but so far only in the lab. Apigenin inhibited CYP1A2, CYP2C9, and CYP3A4 in enzyme and liver microsome studies, and these enzymes metabolize many common medications including warfarin, certain statins, and some calcium channel blockers used to treat hypertension. Whether this raises drug levels in people taking apigenin supplements has not been demonstrated, but anyone on prescription cardiovascular medications should consult their physician before using apigenin supplements [13][14][15][16][17].
Is apigenin safe to take with other supplements like melatonin or magnesium?
Apigenin displaced a benzodiazepine-site ligand in rat brain binding assays (Ki 4 microM), but in cell studies it inhibited GABA-A receptors rather than boosting them and did not act through the benzodiazepine site, and injected rats moved less without showing anxiolytic effects. Combining it with other sedating supplements such as melatonin, valerian, or alcohol is a theoretical concern that warrants caution [22][19][20][18]. Combinations with non-sedating supplements like magnesium are generally considered lower risk, but interactions have not been systematically studied. When stacking supplements for cardiovascular health, discussing the full list with a healthcare provider is the prudent approach.
References
- Chen CC et al. Calcium- and phosphatidylinositol 3-kinase/Akt-dependent activation of endothelial nitric oxide synthase by apigenin. Life sciences (2010). PMID 21034748
- Klider LM et al. Nitric Oxide and Small and Intermediate Calcium-Activated Potassium Channels Mediate the Vasodilation Induced by Apigenin in the Resistance Vessels of Hypertensive Rats. Molecules (Basel, Switzerland) (2024). PMID 39598814
- Clayton ZS et al. Apigenin restores endothelial function by ameliorating oxidative stress, reverses aortic stiffening, and mitigates vascular inflammation with aging. American journal of physiology. Heart and circulatory physiology (2021). PMID 34114892
- Harahap U et al. Current insights and future perspectives of flavonoids: A promising antihypertensive approach. Phytotherapy research : PTR (2024). PMID 38616386
- Atucha NM et al. Effects of Flavonoids in Experimental Models of Arterial Hypertension. Current topics in medicinal chemistry (2022). PMID 34749613
- Yamagata K et al. Dietary polyphenols regulate endothelial function and prevent cardiovascular disease. Nutrition (Burbank, Los Angeles County, Calif.) (2015). PMID 25466651
- Olszanecki R et al. Flavonoids and nitric oxide synthase. Journal of physiology and pharmacology : an official journal of the Polish Physiological Society (2002). PMID 12512693
- Simoncini T et al. Estrogen-like effects of wine extracts on nitric oxide synthesis in human endothelial cells. Maturitas (2011). PMID 21839593
- Cao Y et al. The antihypertensive potential of flavonoids from Chinese Herbal Medicine: A review. Pharmacological research (2021). PMID 34601080
- Alobaidi S et al. Antihypertensive Property of Celery: A Narrative Review on Current Knowledge. International journal of food science (2024). PMID 38505582
- Ajebli M et al. Phytotherapy of Hypertension: An Updated Overview. Endocrine, metabolic & immune disorders drug targets (2020). PMID 31880255
- Tian J et al. Mitochondrial dysfunction in hypertension: mechanistic pathways and therapeutic implications. Functional & integrative genomics (2026). PMID 41656396
- Fei Lin et al. Inhibitory effect of Selaginella doederleinii hieron on human cytochrome P450. Frontiers in Pharmacology (2023). PMID 36874034
- Wang Z et al. Inhibitory Effect of Apigenin on Losartan Metabolism and CYP2C9 Activity in vitro. Pharmacology (2016). PMID 27287328
- Si D et al. Mechanism of CYP2C9 inhibition by flavones and flavonols. Drug metabolism and disposition: the biological fate of chemicals (2009). PMID 19074529
- Shimada H et al. Differential mechanisms for the inhibition of human cytochrome P450 1A2 by apigenin and genistein. Journal of biochemical and molecular toxicology (2010). PMID 20806393
- Kondža M et al. Characterization of the CYP3A4 Enzyme Inhibition Potential of Selected Flavonoids. Molecules (Basel, Switzerland) (2021). PMID 34069400
- Salehi B et al. The Therapeutic Potential of Apigenin. International journal of molecular sciences (2019). PMID 30875872
- Campbell EL et al. The dietary flavonoids apigenin and (-)-epigallocatechin gallate enhance the positive modulation by diazepam of the activation by GABA of recombinant GABA(A) receptors. Biochemical pharmacology (2004). PMID 15451406
- Goutman JD et al. Flavonoid modulation of ionic currents mediated by GABA(A) and GABA(C) receptors. European journal of pharmacology (2003). PMID 12586201
- Venigalla M et al. Curcumin and Apigenin – novel and promising therapeutics against chronic neuroinflammation in Alzheimer's disease. Neural regeneration research (2015). PMID 26487830
- Haydée Viola et al. Apigenin, a Component ofMatricaria recutitaFlowers, is a Central Benzodiazepine Receptors-Ligand with Anxiolytic Effects. Planta Medica (1995). PMID 7617761
- Mao JJ et al. Long-term chamomile (Matricaria chamomilla L.) treatment for generalized anxiety disorder: A randomized clinical trial. Phytomedicine : international journal of phytotherapy and phytopharmacology (2016). PMID 27912875
- Pourshaikhian M et al. Effects of aromatherapy with Matricaria chamomile essential oil on anxiety and hemodynamic indices in patients with acute coronary syndrome, 2021: a randomized controlled trial. BMC complementary medicine and therapies (2024). PMID 38172912
- Yu W et al. Apigenin Attenuates Adriamycin-Induced Cardiomyocyte Apoptosis via the PI3K/AKT/mTOR Pathway. Evidence-based complementary and alternative medicine : eCAM (2017). PMID 28684964
These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.
