Oyster Mushrooms and Inflammation: The Mechanisms

Oyster Mushroom (Pleurotus ostreatus)

2 inflammatory pathways inhibited

Oyster mushroom extract inhibits both NF-kB and AP-1, the two master switches that turn on inflammatory genes. Most anti-inflammatory agents hit only one. The dual inhibition is what separates oyster mushroom's mechanism from simpler anti-inflammatory compounds.

Jedinak et al., Nutrition Journal, 2011

3 cytokines

suppressed in macrophages: TNF-alpha, IL-6, and IL-12p40, alongside prostaglandin E2 and nitric oxide (Jedinak, 2011)

5 species

of Pleurotus compared for antioxidant and anti-inflammatory activity — P. ostreatus led the NF-kB inhibition assay (Stastny, 2022)

Pleuran

the named, standardized beta-glucan from P. ostreatus with its own clinical evidence base

Jedinak et al., Nutrition Journal, 2011

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Oyster mushroom's anti-inflammatory reputation in health media is usually supported by generic language about "beta-glucans" and "immune support." The actual research is more specific and more interesting.

A 2011 mechanistic study found that oyster mushroom (Pleurotus ostreatus) extract suppresses inflammation not through one pathway but two: it simultaneously inhibits NF-kB and AP-1, the two major protein complexes that activate inflammatory gene expression inside cells. Targeting both at once is not how most anti-inflammatory agents work, and it explains why oyster mushroom's effects span multiple inflammatory cytokines rather than just one.

This article is part of our guide to the oyster mushroom species. Here we break down the four distinct mechanisms behind oyster mushroom's anti-inflammatory activity, which species show the strongest effects, and how the laboratory data connects to oral consumption in humans.

The Master Inflammation Switches (and Why Oyster Mushroom Inhibits Two of Them)

Inflammation at the cellular level begins when a threat signal reaches a cell and triggers a cascade that ends with the production of inflammatory proteins: cytokines, enzymes, and signaling molecules that recruit immune cells and amplify the response. The control of this cascade runs through specific protein complexes called transcription factors, which act as switches that turn inflammatory genes on or off.

NF-kB is the most studied of these switches. Proteins that make up the NF-kB complex normally sit dormant in the cell's cytoplasm. When an inflammatory trigger arrives, the complex is released, moves into the cell nucleus, and binds to DNA sequences that activate genes for TNF-alpha, IL-6, and other pro-inflammatory molecules. Nearly every chronic inflammatory disease involves dysregulated NF-kB. Many pharmaceutical anti-inflammatory approaches, from corticosteroids to biologics, work partly by interfering with NF-kB.

AP-1 is a second transcription factor that works alongside NF-kB and independently. Even when NF-kB is blocked, AP-1 can continue driving inflammatory gene expression. An intervention that only targets NF-kB leaves AP-1 partially operational.

Jedinak and colleagues published a mechanistic study in Nutrition Journal in 2011 testing oyster mushroom concentrate in macrophages and in mice.^[2] In RAW264.7 macrophages stimulated with bacterial lipopolysaccharide, the extract suppressed secretion of TNF-alpha, IL-6, and IL-12p40. It also reduced production of prostaglandin E2 and nitric oxide, and gel-shift analysis showed it did so by inhibiting the DNA-binding activity of both AP-1 and NF-kB. Simultaneously inhibiting both transcription factors is mechanistically significant: it means oyster mushroom extract does not leave an inflammatory bypass route open that a single-pathway agent would leave untouched.

Two Switches, Both Blocked

How Oyster Mushroom Concentrate Shuts Down Both Inflammatory Switches

NF-kB and AP-1 run in parallel, so blocking only one leaves the other driving inflammatory gene expression. In LPS-stimulated macrophages, oyster mushroom concentrate inhibited the DNA-binding activity of both, and five separate inflammatory outputs fell.

Note: the macrophage cytokine readouts in this study were TNF-alpha, IL-6 and IL-12p40. IL-1beta is frequently listed in secondary summaries of this work but was not among them — IL-1beta appears instead in the separate P. pulmonarius colitis study (Lavi 2010). All findings here are from murine macrophages, mouse splenocytes and mice; this is preclinical mechanism data, not a human result.

Two details are worth separating carefully, because they are often blurred together in secondary coverage. First, the cytokines Jedinak's team actually measured were TNF-alpha, IL-6, and IL-12p40 — IL-1beta was not among the macrophage readouts, despite frequently appearing in summaries of this study. Second, the study was not purely a cell experiment. Oral administration of the concentrate markedly suppressed TNF-alpha and IL-6 secretion in mice challenged with lipopolysaccharide, and the anti-inflammatory activity was confirmed again in stimulated mouse splenocytes. That in vivo arm matters: it is the strongest single piece of evidence that eating oyster mushroom material, rather than applying it to cells, produces a measurable systemic anti-inflammatory effect.

The cytokines suppressed are relevant targets. TNF-alpha drives systemic inflammatory responses in conditions from rheumatoid arthritis to inflammatory bowel disease. IL-6 is elevated in chronic low-grade inflammation associated with metabolic syndrome and cardiovascular disease. IL-12p40 is a shared subunit of the cytokines that steer T-cell-driven inflammation. Nitric oxide at high concentrations in inflammatory tissue causes direct tissue damage.

Mechanism study

Jedinak, Dudhgaonkar, Wu, Simon, Sliva (2011) · Nutrition Journal

Population

RAW264.7 murine macrophages and mouse splenocytes, plus mice given lipopolysaccharide in vivo

Intervention

Oyster mushroom concentrate (0-100 µg/ml in vitro; oral administration in vivo)

Finding

Suppressed TNF-alpha, IL-6 and IL-12p40, lowered PGE2 and nitric oxide through COX-2 and iNOS downregulation, and inhibited DNA-binding of both AP-1 and NF-kB. Oral dosing suppressed TNF-alpha and IL-6 in mice.

positive Strong, internally consistent preclinical result with a genuine in vivo oral arm. Still animal and cell data — not a human trial.

Jedinak et al., Nutrition Journal, 2011

Adhesion Molecules: The Vascular Inflammation Connection

A second mechanism explains how mushroom extracts reach blood vessel walls, not just soft tissue.

When chronic inflammation is present in the body, blood vessel walls respond by producing adhesion molecules on their inner surface. Two of the most important are ICAM-1 (intercellular adhesion molecule-1) and VCAM-1 (vascular cell adhesion molecule-1). These proteins act like molecular hooks that allow white blood cells circulating in the bloodstream to grab onto the vessel wall, stop their movement, and migrate through into the surrounding tissue. In the artery wall, this process is a central step in the development of atherosclerotic plaques.

Martin published a 2010 study in Nutrition Journal testing whether both common and specialty mushroom extracts could inhibit adhesion molecule expression on human aortic endothelial cells in a pro-inflammatory environment.^[1] Cells were exposed to extracts of white button and crimini (Agaricus bisporus), shiitake, oyster (Pleurotus ostreatus), and maitake, then stimulated with IL-1beta.

The result deserves precision, because it is routinely overstated. White button mushroom was the extract that consistently reduced all three markers — VCAM-1, ICAM-1, and E-selectin-1. The other mushrooms, oyster among them, modulated adhesion molecule expression more selectively, affecting markers singly or in combination rather than across the board. What was true of every mushroom tested, including oyster, was that all of them significantly reduced the binding of monocytes to the endothelial monolayer.

Attribution check

Does oyster mushroom 'shut down' ICAM-1 and VCAM-1?

The claim

“Oyster mushroom extract inhibits the adhesion molecules ICAM-1 and VCAM-1 on blood vessel walls.”

Secondary summaries of Martin's 2010 mushroom panel, which collapse the results of five different mushrooms into a single headline.

What research shows

Overstated

In the study, white button mushroom was the extract that consistently lowered ICAM-1, VCAM-1 and E-selectin-1. Oyster mushroom modulated adhesion molecules more selectively, not uniformly across all three.

The finding that did hold for oyster mushroom is arguably the more functionally meaningful one: every mushroom tested significantly reduced monocyte binding to the endothelium, which is the downstream event adhesion molecules exist to enable. This is cell-culture work, not evidence of an effect on human arteries.

Martin, Nutrition Journal, 2010

This adhesion mechanism still connects mushroom consumption to cardiovascular biology, and it is distinct from the NF-kB cytokine mechanism. But the honest version of the claim is that oyster mushroom reduced monocyte adhesion, not that it broadly suppressed adhesion molecule expression. For the cardiovascular research specifically, see our review of oyster mushrooms and heart health.

The Antioxidant Upstream Pathway: Breaking the Inflammation Cycle Early

NF-kB activation does not require a direct inflammatory signal. Oxidative stress, the buildup of reactive oxygen molecules in cells, is itself a potent NF-kB activator. Cells under oxidative stress read that stress as a threat signal and initiate the NF-kB inflammatory cascade. This creates a self-reinforcing cycle: oxidative stress triggers inflammation, which produces more reactive oxygen species, which maintain oxidative stress, which keeps NF-kB active.

Oyster mushrooms are rich in antioxidant compounds including ergothioneine, a sulfur-containing amino acid produced almost exclusively by fungi that concentrates in human tissues. Oyster mushrooms are among the highest dietary sources of ergothioneine. They also contain phenolic compounds that scavenge reactive oxygen molecules directly.

Kleftaki and colleagues published a randomized controlled trial in Antioxidants in 2022 that provides the clearest human data in this article.^[7] One hundred metabolically unhealthy patients were randomized for three months. Both groups received conventional nutritional counseling; the intervention group additionally ate a daily baked, UV-B-irradiated P. eryngii (king oyster) mushroom snack. Compared with the control group, the snack regulated glucose levels and reduced body weight, fat, and waist and hip circumference. Within the intervention group, LDL and SGOT fell, vitamin D2 status rose, and — most relevant here — IL-6 and oxidized LDL both decreased.

That result does two things for the mechanistic story. It confirms the antioxidant arm in humans, via oxidized LDL, a marker of oxidative damage to lipoproteins. And it delivers a human anti-inflammatory readout, IL-6, which is one of the same cytokines Jedinak's team saw suppressed in macrophages and mice. The upstream and downstream halves of the mechanism both register in living people, not just in culture.

This upstream antioxidant mechanism complements the direct NF-kB inhibition: one pathway blocks the inflammatory switches after they have been triggered; the other reduces one of the upstream signals that triggers those switches in the first place. For more on the antioxidant chemistry specifically, see our article on oyster mushroom antioxidants.

Which Oyster Mushroom Species Has the Strongest Anti-Inflammatory Effect?

"Oyster mushroom" is not a single species. The commercial category includes Pleurotus ostreatus (pearl oyster), Pleurotus eryngii (king oyster, also called king trumpet), Pleurotus pulmonarius (phoenix oyster), Pleurotus djamor (pink oyster), and Pleurotus citrinopileatus (golden oyster), among others. The research does not treat them as interchangeable.

Stastny and colleagues published a 2022 study in Antioxidants comparing the antioxidant and anti-inflammatory activity of five medicinal mushrooms of the genus Pleurotus, with a deliberate focus on lesser-known species alongside the familiar P. ostreatus.^[4] They prepared multiple extracts per species and characterized them by HPLC-HRMS, GC-MS, and NMR.

Their headline finding is that activity is split, not concentrated in one species — and that it depends as much on the extract as on the mushroom. The 80% methanol extract of P. ostreatus Florida was the most active in the NF-kB inhibition assay, and it also had the highest beta-glucan content at 43.3% by dry weight. But P. flabellatus was the most active radical scavenger, with the highest ORAC value and the highest levels of ergosterol, ergothioneine, and mannitol, and it was a P. flabellatus chloroform extract that showed significant anti-inflammatory COX-2 activity.

Five Species Compared, Result Split

No Single Pleurotus Species Won Every Measure

When five Pleurotus species were tested head to head, the antioxidant crown and the NF-kB crown went to different species — and to different solvent extracts of them. That split is the finding. Any claim that one oyster mushroom is simply "the most anti-inflammatory" is collapsing two separate results into one.

Leads on NF-kB inhibition

P. ostreatus Florida

80% methanol extract

• NF-kB inhibition assay: Most active of the set
• Beta-glucan content: 43.3% by dry weight (highest)

This is the lane that supports the article’s central mechanism claim — but it is specifically the NF-kB assay, not anti-inflammatory activity in general.

Leads on antioxidant and COX-2

P. flabellatus

methanol + chloroform extracts

• Radical scavenging / ORAC: Most active, highest ORAC
• COX-2 anti-inflammatory activity: Significant (chloroform extract)
• Ergothioneine, ergosterol, mannitol: Highest levels

The authors singled out this lesser-known species as the one whose therapeutic potential most warrants further investigation.

Activity also tracked the extraction solvent, not just the mushroom: the same species gave different results in methanol versus chloroform. This is extract chemistry measured in the laboratory — it does not tell you what a cooked mushroom or a commercial supplement delivers.

So the accurate statement is narrow: within this comparison, P. ostreatus led on NF-kB inhibition specifically. It was not the strongest performer on every anti-inflammatory or antioxidant measure. The authors' own conclusion pointed toward P. flabellatus as the species most worth further investigation. Any claim that one Pleurotus species is simply "the most anti-inflammatory" collapses a genuinely split result.

Kim and colleagues published a 2017 study in the International Journal of Medicinal Mushrooms on the immunomodulatory effects of an extracellular beta-glucan isolated from P. eryngii (king oyster) and its sulfated form, examining signaling molecules involved in innate immunity.^[3] The work illustrates that glucans from different Pleurotus species — and even chemically modified versions of the same glucan — engage innate immune signaling differently, which is the molecular reason species substitution is not neutral.

P. pulmonarius contributes evidence for the oral consumption pathway. Lavi and colleagues published a 2010 study in the British Journal of Nutrition in which glucan preparations from P. pulmonarius were fed daily to mice with colitis induced by dextran sulfate sodium.^[6] The orally administered glucans attenuated and helped prevent colitis symptoms: they blocked colon shortening, suppressed myeloperoxidase activity, improved macroscopic and histological damage scores, significantly decreased TNF-alpha protein in colonic tissue, and attenuated the elevated expression of IL-1beta.

It is worth being precise about what this model does and does not show. Dextran sulfate sodium colitis is a disease of the gut, and the glucans were eaten, so this is evidence that orally consumed Pleurotus glucans retain anti-inflammatory activity in the intestinal tract — a meaningful result for inflammatory bowel conditions specifically. It is not evidence of a systemic effect reaching distant tissue. The strongest support for the oral-to-systemic route remains the in vivo arm of Jedinak's study, where oral oyster mushroom concentrate suppressed circulating TNF-alpha and IL-6 in mice challenged systemically.

Practically, this species variation means supplement products and fresh mushrooms using different Pleurotus species have potentially different profiles. Studies on P. ostreatus do not automatically apply to products containing P. eryngii or P. pulmonarius.

What the Evidence Looks Like From Cell Study to Human Trial

The mechanistic core of this article — dual NF-kB/AP-1 inhibition, adhesion molecule modulation, the species comparison — is preclinical. Jedinak's study adds a mouse in vivo arm; Lavi's is a mouse colitis model; Martin's and Stastny's are cell and extract work.

The human evidence comes from two directions. The first is Pleuran, the standardized 1,3/1,6-beta-glucan extracted from P. ostreatus. Bergendiova and colleagues ran a double-blind, placebo-controlled trial in which fifty athletes took pleuran or placebo for three months.^[5] Pleuran significantly reduced the incidence of upper respiratory tract infection symptoms and increased circulating natural killer cell counts, and phagocytosis remained stable in the pleuran group while it declined significantly in the placebo group. Bobovcak and colleagues reported a complementary result on cellular immune response after intensive exercise in elite athletes.^[8] These are immune-function trials rather than inflammation trials, but they establish that oral oyster mushroom beta-glucan produces measurable immunological change in humans.

The second is the Kleftaki trial described above, which is the closest thing in this literature to a direct human anti-inflammatory result for an oyster mushroom: a three-month randomized controlled trial in which a P. eryngii snack lowered IL-6 and oxidized LDL.^[7]

For the full Pleuran clinical picture, see our Pleuran cytokine modulation article.

Evidence reach

1. Cell studiescompleted

   Dual NF-kB and AP-1 DNA-binding inhibition; suppressed TNF-alpha, IL-6, IL-12p40, PGE2, NO (Jedinak 2011). Adhesion molecule and monocyte binding work (Martin 2010). Five-species extract comparison (Stastny 2022).

2. Animal studiescompleted

   Oral oyster mushroom concentrate suppressed TNF-alpha and IL-6 in LPS-challenged mice (Jedinak 2011). Oral P. pulmonarius glucans reduced colonic TNF-alpha and IL-1beta in DSS colitis (Lavi 2010).

3. Small human trialscurrent

   Pleuran reduced upper respiratory infection incidence and preserved immune cell function in 50 athletes (Bergendiova 2011; Bobovcak 2010). A P. eryngii snack lowered IL-6 and oxidized LDL in 100 metabolically unhealthy adults (Kleftaki 2022).

4. Large RCTsmissing

   No large trial has tested oyster mushroom against a defined inflammatory disease endpoint.

5. Meta-analysismissing

   No meta-analysis of oyster mushroom anti-inflammatory outcomes exists.

The mechanism is well characterized in cells and reproduced in mice, including by the oral route. Human evidence has reached the small-trial tier: IL-6 and oxidized LDL fell in a 100-person RCT, and Pleuran has repeatable immune-function results in athletes. What does not exist is a large trial testing oyster mushroom against a clinical inflammatory disease endpoint.

Jedinak 2011; Martin 2010; Lavi 2010; Bergendiova 2011; Bobovcak 2010; Stastny 2022; Kleftaki 2022

The honest position: the dual NF-kB/AP-1 inhibition is preclinical, with a supporting oral in vivo arm in mice. The adhesion molecule work is in cell culture, and oyster mushroom's contribution there is reduced monocyte binding rather than broad adhesion molecule suppression. Human data now includes a measured drop in IL-6, so it is no longer accurate to say that no human trial has recorded an anti-inflammatory cytokine change after oyster mushroom consumption. What remains absent is a trial in people with a diagnosed inflammatory condition, measuring disease outcomes rather than biomarkers.

Practical context

Moderate

Mechanism evidence is not a treatment plan

Concern

Oyster mushroom's anti-inflammatory mechanisms are documented mostly in cells and mice. Treating culinary or supplemental oyster mushroom as a substitute for prescribed anti-inflammatory or disease-modifying therapy is not supported by the evidence described here.

What the research says

Oyster mushrooms are a well-tolerated food, and eating them is reasonable for general dietary reasons. Any use aimed at a diagnosed inflammatory condition should be discussed with the clinician managing that condition, and added alongside existing treatment rather than in place of it.

Particularly relevant for: People with autoimmune disease, those taking immunosuppressants, and anyone with a diagnosed mushroom allergy warrant particular caution, since beta-glucans act by modulating immune signaling rather than simply suppressing it.

What to do

Treat this article as mechanism education, not medical advice. Do not stop or change prescribed medication based on it.

Jedinak 2011; Lavi 2010; Kleftaki 2022

For the joint health and arthritis research, where the anti-inflammatory mechanisms have specific implications, see oyster mushroom and joint inflammation and oyster mushroom for chronic inflammatory conditions.

The Bottom Line

Oyster mushroom's anti-inflammatory activity operates through four distinct mechanisms: dual inhibition of the NF-kB and AP-1 inflammatory switches, modulation of adhesion molecules and monocyte binding at the vessel wall, antioxidant activity that breaks the oxidative stress-to-inflammation cycle, and beta-glucan signaling through innate immune receptors. Within a five-species Pleurotus comparison, P. ostreatus led specifically on NF-kB inhibition, while P. flabellatus was the strongest antioxidant and carried the COX-2 activity. The strongest human evidence is a 2022 randomized controlled trial in which a P. eryngii snack lowered IL-6 and oxidized LDL in 100 metabolically unhealthy adults, alongside Pleuran trials showing immune effects in athletes. No large trial has yet tested oyster mushroom against a clinical inflammatory disease endpoint.

Frequently Asked Questions

Is oyster mushroom anti-inflammatory?

Yes, with mechanistic evidence across multiple pathways. A 2011 study found oyster mushroom extract inhibits the DNA-binding activity of both NF-kB and AP-1, the two major protein complexes that turn on inflammatory gene expression, reducing TNF-alpha, IL-6, IL-12p40, prostaglandin E2 and nitric oxide in macrophages — and oral dosing suppressed TNF-alpha and IL-6 in mice (Jedinak et al., 2011). In humans, a 2022 randomized controlled trial found a P. eryngii mushroom snack lowered IL-6 and oxidized LDL over three months in 100 metabolically unhealthy adults (Kleftaki et al., 2022). What does not yet exist is a trial in people with a diagnosed inflammatory disease.

What makes oyster mushrooms anti-inflammatory?

Several compound classes contribute. Beta-glucans, including the standardized 1,3/1,6-beta-glucan known as Pleuran, modulate innate immune signaling. Ergothioneine, a sulfur-containing antioxidant that fungi produce and human tissues concentrate, neutralizes reactive oxygen species upstream of inflammation. Phenolic compounds add further antioxidant activity. In the five-species Pleurotus comparison, the extract with the highest beta-glucan content (43.3% by dry weight, from P. ostreatus Florida) was also the most active in the NF-kB inhibition assay, while the extract richest in ergothioneine and ergosterol (P. flabellatus) was the strongest radical scavenger (Stastny et al., 2022).

How do oyster mushrooms reduce inflammation?

Through dual NF-kB and AP-1 inhibition — blocking the DNA-binding activity of both protein complexes that activate inflammatory gene expression, which lowers TNF-alpha, IL-6 and IL-12p40 and reduces prostaglandin E2 and nitric oxide via COX-2 and iNOS downregulation (Jedinak et al., 2011). Antioxidant compounds separately reduce oxidative stress, an upstream trigger for NF-kB activation. Mushroom extracts also reduce monocyte binding to blood vessel walls in cell culture (Martin, 2010). A 2022 human RCT found measurable reductions in IL-6 and oxidized LDL from P. eryngii supplementation (Kleftaki et al., 2022).

Which mushroom is the most anti-inflammatory?

There is no clean answer, and the best available comparison shows why. A 2022 study comparing five Pleurotus species found the result was split: P. ostreatus Florida was most active in the NF-kB inhibition assay, while P. flabellatus had the highest antioxidant capacity and carried the significant COX-2 anti-inflammatory activity (Stastny et al., 2022). Across all mushroom genera the picture is more complex still, since lion's mane, reishi and turkey tail each act through different pathways. No head-to-head human trial comparing anti-inflammatory potency across mushroom species has been published.

Do oyster mushrooms contain beta-glucan?

Yes. Oyster mushrooms are rich in 1,3/1,6-beta-glucans, with Pleuran being the specific named and standardized extract from Pleurotus ostreatus. Content varies substantially by species, cultivation method, and extraction approach — one extract in the 2022 five-species comparison reached 43.3% beta-glucan by dry weight (Stastny et al., 2022). Fresh oyster mushrooms contain beta-glucans as part of their cell wall structure, and the amount reaching systemic immune tissue from food differs from purified Pleuran supplements, which is what the human athlete trials actually tested (Bergendiova et al., 2011).

Sources & References

1. 1RTHM-00354·Martin, Keith R (2010). “Both common and specialty mushrooms inhibit adhesion molecule expression and in vitro binding of monocytes to human aortic endothelial cells in a pro-inflammatory environment..” Nutrition journal.Study breakdown →PubMed →↩
2. 2RTHM-00219·Jedinak, Andrej et al. (2011). “Anti-inflammatory activity of edible oyster mushroom is mediated through the inhibition of NF-κB and AP-1 signaling..” Nutrition journal.Study breakdown →PubMed →↩
3. 3RTHM-00883·Kim, Yong Hyun et al. (2017). “Immunomodulatory Effects of Extracellular β-Glucan Isolated from the King Oyster Mushroom Pleurotus eryngii (Agaricomycetes) and Its Sulfated Form on Signaling Molecules Involved in Innate Immunity..” International journal of medicinal mushrooms.Study breakdown →PubMed →↩
4. 4RTHM-01618·Stastny, Jan et al. (2022). “Antioxidant and Anti-Inflammatory Activity of Five Medicinal Mushrooms of the Genus Pleurotus..” Antioxidants (Basel.Study breakdown →PubMed →↩
5. 5RTHM-00379·Bergendiova, Katarina et al. (2011). “Pleuran (β-glucan from Pleurotus ostreatus) supplementation, cellular immune response and respiratory tract infections in athletes..” European journal of applied physiology.Study breakdown →PubMed →↩
6. 6RTHM-00190·Lavi, Iris et al. (2010). “Orally administered glucans from the edible mushroom Pleurotus pulmonarius reduce acute inflammation in dextran sulfate sodium-induced experimental colitis..” The British journal of nutrition.Study breakdown →PubMed →↩
7. 7RTHM-00771·Kleftaki, Stamatia-Angeliki et al. (2022). “A Randomized Controlled Trial on Pleurotus eryngii Mushrooms with Antioxidant Compounds and Vitamin D2 in Managing Metabolic Disorders..” Antioxidants (Basel.Study breakdown →PubMed →↩
8. 8RTHM-00327·Bobovčák, Marián et al. (2010). “Effect of Pleuran (β-glucan from Pleurotus ostreatus) supplementation on cellular immune response after intensive exercise in elite athletes..” Applied physiology.Study breakdown →PubMed →↩