Methylene Blue and the Immune System: Mechanisms, Evidence, and Considerations

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Methylene blue modulates immunity by inhibiting iNOS/NO signalling, suppressing NF-κB and inflammasome activation, and reducing the production of IL-1β, IL-18, IL-6, and MCP-1. It stabilises mitochondrial respiration as an alternative electron carrier, lowers ROS, and boosts ATP, aiding immune cell energetics.

It tempers macrophage/neutrophil activation, as well as MMP release. Clinically, it treats methemoglobinemia and shows signals in severe COVID-19.

Safety constraints include serotonin syndrome risk and G6PD deficiency.

Dosing ranges from 0 to –2.0 mg/kg/h with monitoring. Further data clarifies the scope and strategy.

Key Takeaways

Methylene blue downregulates iNOS/NO signalling, thereby tempering macrophage and neutrophil activation and reducing pro-inflammatory mediators, such as chemokines and MMP-2/MMP-9.
It suppresses NF-κB and inflammasome activity, lowering IL-1β, IL-18, IL-6, and MCP-1 by reducing mitochondrial ROS and limiting priming and activation phases.
As a mitochondrial electron carrier and antioxidant, it stabilises respiration, enhances complex IV activity, and boosts ATP production, supporting the energy needs of immune cells.
Clinically, it treats methemoglobinemia and shows benefit in severe COVID-19 trials, but risks include serotonin syndrome, seizures, and cardiovascular complications.
Dosing requires careful monitoring (MAP, lactate, oxygenation); it is contraindicated in G6PD deficiency. More randomised, dose-ranging trials are needed to define the immunomodulatory effects of this treatment.

Anti-Inflammatory Mechanisms and Immune Modulation

Precision emerges when methylene blue (MB) is examined through its anti-inflammatory and immunomodulatory actions. MB downregulates inducible nitric oxide synthase, thereby suppressing iNOS/NO-dependent inflammatory signalling, and concurrently inhibits neuronal nitric oxide synthase and soluble guanylyl cyclase, resulting in extensive suppression of the NO pathway.

Resultant NO reduction limits vasodilation, dampens peripheral inflammatory activation, and contributes to analgesia in osteoarthritis and colitis models, supporting therapeutic potential. In osteoarthritis models, intra-articular MB increased MEG3 expression while reducing P2X3 levels, aligning with improved weight distribution and decreased swelling.

Methylene blue suppresses NO pathways, easing inflammation and pain, revealing therapeutic promise across inflammatory disorders.

MB also protects mitochondria during inflammatory stress by bypassing impaired electron transport segments to sustain ATP generation, preserving membrane integrity, and reducing bioenergetic failure. Enhanced mitochondrial efficiency lowers cellular stress signals and curtails downstream inflammatory burden.

As a redox-active agent, MB scavenges reactive oxygen species, limiting oxidative injury to mitochondria and adjacent tissues and preventing escalation of damage-associated inflammation. As part of its historical development, MB was first used in the textile industry before its medical applications were recognised.

At the cellular interface, MB mediates immune modulation by tempering macrophage and neutrophil activation, altering migratory behaviour, and restricting the release of pro-inflammatory mediators, including chemokines and MMP-2/MMP-9, while elevating cytoprotective factors such as PEDF.

In clinical practice, MB is considered safe at low doses and is contraindicated in G6PD deficiency.

Cytokine Regulation and Inflammatory Signalling Pathways

Although classically described as a redox dye, methylene blue exerts targeted control over cytokine networks by interrupting core inflammatory signalling nodes. It suppresses cytokine signalling by converging on inflammasome, NF-κB, STAT3, and nitric oxide-dependent pathways, thereby constraining the production of inflammatory mediators.

Methylene blue inhibits canonical and non-canonical inflammasome activation, limiting assembly, phagocytosis, and transcription of NLRP3, NLRC4, and AIM2 components. Reduced mitochondrial ROS and diminished caspase-1 activity prevent the maturation of IL-1β and IL-1α, accompanied by lowered NLRP3 promoter activity in macrophages. In animal models, methylene blue improved survival in septic mice, highlighting its potential therapeutic impact on inflammasome-driven pathology.

As secondary damage in spinal cord injury unfolds over minutes to weeks, modulating neuroinflammation may help limit downstream neuronal loss.

Upstream, it blunts NF-κB activation, decreasing NF-κB binding to the iNOS promoter and disrupting the iNOS/NO–NF-κB feed-forward loop. By preventing NF-κB-driven cytokine gene expression, it attenuates IL-1α, IL-1β, IL-6, IL-10, G-CSF, MCP-1, MIP-1α, and MIP-1β, including microglial releases under LPS. As a clinically established therapy, methylene blue treats methemoglobinemia, illustrating its capacity to modulate hemoprotein function and redox balance.

Concurrently, inhibition of iNOS, nNOS, eNOS, and sGC–cGMP signalling suppresses NO-dependent inflammatory cascades. Tissue-specific STAT3 inhibition following LPS correlates with sustained serum cytokine reductions, reinforcing the control of a multi-node pathway.

Mitochondrial Protection and Cellular Energy Support

Mobilising its redox cycling capacity, methylene blue safeguards mitochondrial function by serving as an alternative electron carrier that stabilises respiration under stress conditions. Low-dose exposure redirects electrons from NADH to cytochrome c, thereby augmenting complex IV activity and facilitating oxygen reduction to water.

Preferential formation of redox cycling complexes in neuronal mitochondria preserves mitochondrial dynamics and maintains energy homeostasis when segments of the electron transport chain are impaired. By ensuring a steady electron flux, it optimises ADP phosphorylation, increases oxygen consumption, and supports ATP content both in vitro and in vivo.

Methylene blue also acts as a potent antioxidant within mitochondria, helping reduce oxidative stress that can otherwise impair cellular energy systems. At low doses, methylene blue can boost ATP production by approximately 30%, reflecting its role in enhancing mitochondrial output. Both methylene blue and near-infrared light increase cytochrome oxidase expression and mitochondrial respiration, supporting long-term neuroprotective metabolic capacity.

This bypass mechanism prevents catastrophic ATP collapse during metabolic insults, thereby sustaining essential neuronal functions, including synaptic transmission and calcium buffering. Evidence from stroke and brain injury models indicates increased cytochrome oxidase activity, enhanced oxygen uptake, and preserved mitochondrial respiration, which aligns with observed improvements in cerebral perfusion in hypoperfused tissue.

Collectively, these actions stabilise the cellular energy supply, strengthen the neuronal metabolic infrastructure, and support resilience under both physiological and pathological stressors.

Antioxidant Actions and Redox Balance

Methylene blue exhibits high radical scavenging efficiency by directly quenching mitochondrial reactive oxygen species and stabilising membrane, protein, and DNA targets against oxidative modification.

Its reversible redox cycling between oxidised and reduced forms enables catalytic regeneration of antioxidant capacity across various cellular environments, sustaining redox homeostasis under metabolic and environmental stressors.

Evidence indicates that this bidirectional electron shuttling both limits cumulative oxidative damage and preserves immune-relevant mitochondrial function without impairing antimicrobial ROS signalling. Supporting immune cell energy demands helps maintain efficient pathogen recognition and elimination through enhanced immune cell function.

As an FDA-approved therapy for methemoglobinemia, it also enhances haemoglobin’s oxygen-carrying capacity, thereby indirectly supporting tissue oxygenation during immune activation.

Radical Scavenging Efficiency

At low concentrations, this phenothiazine dye enhances redox balance by catalytically rerouting mitochondrial electron flow to curb radical generation and scavenge reactive species.

By accepting electrons from NADH at Complex I and donating them directly to cytochrome c as leucoMB, it limits superoxide formation at Complex I/III, attenuating oxidative stress and shaping radical interactions. In photocatalytic systems, LDH@g-C heterostructures enhance charge separation and reduce electron–hole recombination, thereby improving dye degradation efficiency.

The low redox potential (~11 mV) supports rapid, reversible cycling, which sustains cytochrome oxidase activity and ATP production while reducing the ROS burden. The EF-PMS process has demonstrated effectiveness in varying water quality backgrounds, underscoring the versatility of reactive oxygen species generation pathways that can be modulated across different matrices. On iron-amended granular activated carbon, staged H2O2 applications in heterogeneous Fenton oxidation can increase dye removal efficiency to nearly 100% while minimising radical scavenging.

Electron spin resonance confirms concurrent radical species in degradation settings, where •OH, SO4˙−, and 1O2 predominate and are modulated by matrix components.

Bypass of Complex I/III lowers primary ROS generation.
LeucoMB→cytochrome c electron transfer is catalytic.
•OH scavengers (tert-butanol, acetonitrile, CaCO3) suppress reactions.
H2O2 dosing enhances removal efficiency to 100%.
Bicarbonate radicals extend oxidative lifetimes.

Redox Cycling Dynamics

Building on Complex I/III bypass and catalytic leucoMB→cytochrome c transfer, redox cycling emerges as a sustained antioxidant mechanism that buffers electron pressure at its source.

Methylene blue interconverts between MBox and MBred via ECC schemes, operating as a rechargeable antioxidant rather than a sacrificial scavenger. Its delocalised π-system and structural stability permit repeated electron shuttling under oxidative stress.

Thermodynamic profiling reveals an endergonic interaction with Ru(NH3)6³⁺ and a highly exergonic reduction by TCEP, enabling directionally controlled cycles.

In mitochondria, MBred donates electrons to cytochrome c and supports cytochrome c oxidase activity, thereby elevating oxygen consumption (up to 70%) and ATP production (~30%), while maintaining redox balance.

Persistent redox cycling limits ROS generation upstream, integrates with ETC contingencies, and underlies the compound’s therapeutic potential in oxidative pathologies.

Effects on Macrophages, Neutrophils, and Immune Cell Function

Methylene blue directly modulates innate effector cells, suppressing macrophage activation programs and cytokine output while altering neutrophil chemotaxis.

Evidence indicates the inhibition of NF-κB/STAT3 signalling, reduced NLRP3 inflammasome activity (resulting in lower IL-1β and caspase-1 levels), and diminished IL-6, collectively reprogramming inflammatory set points.

Concomitant interference with NO–cGMP signalling and vascular tone further restricts neutrophil trafficking, thereby reinforcing controlled migration and tempering macrophage-driven amplification.

Modulating Macrophage Activation

Although classically defined as a redox-active dye, methylene blue modulates macrophage activation through the convergent regulation of inflammasome signalling, metabolic flux, and cell-death programs, with downstream effects on neutrophils and innate immune function.

It promotes macrophage plasticity via metabolic reprogramming—stimulating the hexose monophosphate shunt, reoxidising NADPH, and triggering a phagocytosis-independent metabolic burst that scales with concentration and drives delayed plasminogen activator release.

Concurrently, it suppresses NLRP3, NLRC4, AIM2, and non-canonical inflammasomes by limiting ASC assembly and caspase-1 cleavage, lowering IL-1β/IL-18 through NF-κB inhibition, while activating Nrf2/HO-1.

Inhibits inflammasome priming and assembly in macrophages and microglia.
Decreases cleaved IL-1β and IL-18 during inflammatory stimulation.
Initiates mitochondrial apoptosis under photodynamic conditions via caspase-9/3.
Restrains pyroptosis through dual-pathway regulation.
Couples antioxidant Nrf2/HO-1 signalling to anti-inflammasome effects.

Neutrophil Migration Control

Under photodynamic conditions, methylene blue often reshapes neutrophil trafficking by altering adhesion dynamics, oxidative tone, and endothelial interactions in a dose- and light-dependent manner.

MB-PDT enhances neutrophil adhesion without triggering myeloperoxidase release, indicating that adhesion reinforcement occurs independently of canonical activation pathways.

LED-driven excitation of intracellular dye elevates reactive oxygen species, generated via photosensitiser activation rather than phagocytic oxidase, thereby modifying membrane avidity and integrin function that guide neutrophil behaviour.

These shifts translate into changed migration patterns across endothelium, with transendothelial migration modulated by both neutrophil-intrinsic ROS and direct endothelial responses to methylene blue, each showing dose–time dependencies.

While viability persists, functional portfolios diverge; notably, impairment of phagocytic machinery curtails candidacidal activity, introducing a trade-off between controlled trafficking and compromised antimicrobial capacity during MB-PDT.

NF-κB, Inflammasomes, and Downstream Signalling Control

Crosstalk between NF-κB signalling and inflammasome activation emerges as a central axis modulated by methylene blue (MB) to blunt macrophage inflammatory responses.

Through NF-κB modulation and inflammasome feedback control, MB interrupts the priming and activation steps. MB suppresses NF-κB binding at the iNOS promoter, lowers iNOS transcription, and limits NO production, thereby preserving Sirt1 from S-nitrosylation and reducing p53 and NF-κB activation.

MB tempers priming and activation: dampened NF-κB–iNOS axis preserves Sirt1, curbing p53 and NF-κB activity.

Concomitantly, MB diminishes mitochondrial ROS, rescues electron transport chain function, and restrains lysosomal permeabilisation, thereby attenuating NLRP3, NLRC4, and AIM2 inflammasomes, caspase-1 activity, and IL-1β secretion.

Transcriptional repression of the NLRP3 promoter further constrains the feed-forward loop.

Reduced rotenone-driven ROS curtails signal 2 for inflammasome assembly
Lower NO maintains Sirt1 activity, decreasing NF-κB–dependent cytokine transcription
Blocked phagocytosis limits crystal uptake, preventing cathepsin B release
Suppressed caspase-1 activation decreases IL-1β maturation and pyroptotic drive
Downregulated iNOS breaks amplification cycles of inflammatory mediators

Collectively, MB converges on priming, activation, and downstream effector phases to compress inflammatory output.

Viral Infections and COVID-19: Mechanistic Insights

Building on its restraint of NF-κB priming and inflammasome activation, methylene blue (MB) interferes with multiple stages of the viral lifecycle relevant to SARS-CoV-2.

At the cell surface, MB inhibits viral entry by blocking spike–ACE2 binding with low micromolar potency (IC50 ≈ 3 μM), corroborated by ELISA-style assays and ACE2-expressing pseudovirus systems (IC50 ≈ 3.5 μM).

Within endocytic compartments, neutral/leuco-MB, a weak base (pKa ~ 9), traverses membranes and transiently alkalises endosomes, thereby impeding maturation steps that require acidic pH and hindering the cytosolic import of virions.

Post-entry, MB’s cationic, planar scaffold intercalates viral RNA, disrupting translation and RNA replication.

As a Zn2+ ionophore, it can impair RdRp elongation, limiting ORF1a/1b translation and downstream pp1a/pp1ab production.

MB also engages SARS-CoV-2 Mpro, obstructing proteolytic processing of non-structural proteins essential for replication.

Extracellularly, MB exhibits direct virucidal effects (EC50 ≈ 0.15 μM), with genomic RNA degradation enhanced by light and exposure time.

Clinical Evidence, Safety Profile, and Dosing Considerations

Clinical evidence spans established indications, such as methemoglobinemia, and adjunctive use in severe COVID-1,9 where randomised trials report improved oxygenation, reduced length of stay, and lower mortality with combination syrup formulations.

Safety is conditional on contraindications and interactions: G6PD deficiency, pregnancy/lactation, MAO inhibition with risk of serotonin syndrome (notably with SSRIs/MAOIs), and dose-related hypertension and cardiotoxicity.

The dosing strategy prioritises micromolar-range exposure for antiviral activity and standard medical dosing for hematologic targets, with monitoring of neurologic status, hemodynamics, and drug–drug interactions to prevent toxicity above approximately 7 mg/kg.

Established Clinical Applications

Although historically known as a redox dye, methylene blue holds well-defined clinical utility anchored by regulatory approvals and mechanistic plausibility. Its principal FDA indication is the treatment of methemoglobinemia, where the compound acts as an NADPH-dependent electron shuttle, reducing Fe3+ to Fe2+ in haemoglobin, thereby rapidly reversing tissue hypoxia and cyanosis.

EMA authorisation corroborates the benefit in acute acquired cases, including drug-induced states from dapsone, benzocaine, nitrites, and environmental sources. Beyond emergency use, blood product sterilisation utilises photosensitised methylene blue to inactivate enveloped viruses in plasma before transfusion, thereby preserving hemostatic function.

Restores oxygen delivery by accelerating methaemoglobin reduction kinetics
Objective signs improve in minutes; urine discolouration may persist transiently
Supports refractory vasoplegic syndrome via inhibition of soluble guanylate cyclase
Aids intraoperative mapping of sentinel lymph nodes and parathyroid visualisation
Reverses ifosfamide-induced encephalopathy through redox modulation of toxic metabolites

Safety Profile and Risks

Despite its established therapeutic roles, methylene blue exhibits a constrained therapeutic index, with risks that reflect its pharmacology as a potent, reversible monoamine oxidase A inhibitor and a redox-active agent.

Principal safety concerns include neurological risks: FDA warnings highlight severe events, notably serotonin syndrome with SSRIs, SNRIs, or tricyclics, plus seizure-like activity, neuromuscular hyperactivity, and mental status changes.

Haematological effects encompass hemolysis, hemolytic anaemia, paradoxical methemoglobinemia, dose-dependent reductions in RBCs, and hyperbilirubinemia.

Cardiovascular complications include hypertension, palpitations, and tachycardia.

Drug interactions are extensive and incompletely mapped, reflecting MAO-A inhibition and other mechanisms.

Toxicity levels are dose-dependent, with escalating gastrointestinal, respiratory, and dermatological symptoms, including necrosis and phototoxicity, as well as higher rates of discontinuation.

In special populations, pediatric patterns often mirror those of adults; heterogeneous data and limited toxicology sustain controversy.

Dosing Strategies and Monitoring

While multiple regimens are reported, the dosing of methylene blue in distributive shock centres on three strategies—single bolus, continuous infusion, and bolus followed by infusion—with continuous infusion being most frequently employed and bolus-plus-infusion linked to lower 28-day mortality in observational data.

Dosing considerations include weight-based infusions of 0.5–2.0 mg/kg/h, fixed bolus protocols (1–4 mg/kg), and recognition that hemodynamic effects are dose-dependent yet transient (~2 hours). A large volume of distribution and prolonged half-life complicate prediction, favouring titration to physiologic endpoints and reassessment within six hours.

Monitoring strategies prioritise maintaining mean arterial pressure, reducing vasoactive medication doses, enhancing lactate clearance, and optimising the PaO2/FiO2 ratio.

Target MAP rise of ~5–6 mmHg post-dose
Evaluate catecholamine-sparing effect
Track heart rate and oxygenation
Limit duration to ≤24 hours; consider repeats
Use models to anticipate non-response

Applications Across Inflammation-Linked Diseases

Across inflammation-linked conditions, methylene blue exerts convergent immunometabolic actions that translate into disease-modifying potential. Within inflammatory diseases, therapeutic strategies converge on the suppression of inflammasome signalling, redox restoration, and modulation of the nociceptive pathway.

Methylene blue unifies immunometabolic actions—dampening inflammasomes, restoring redox balance, and modulating nociception—to reshape inflammatory disease trajectories.

In viral contexts, it inhibits macrophage NLRP3 assembly and attenuates downstream cytokine production, addressing IL-6–centric responses and oxidative stress observed in COVID-19 and post-viral syndromes; mitochondrial efficiency improvements parallel symptom improvements in long-COVID.

In osteoarthritis models, intra-articular dosing (1 mg/kg weekly) limits synovitis, reduces CGRP accumulation, and protects cartilage via Nrf2 and PRDX1 targeting, preventing structural progression while alleviating pain.

Analgesic effects extend to discogenic low back pain, supported by the inhibition of nitric oxide synthase and decreased nitric oxide production; an oral rinse formulation reduces chronic oral pain without the need for local anaesthesia.

Systemically, methylene blue decreases IL-6 levels, suppresses STAT3 activation, and dampens nitric oxide–driven inflammation in osteoarthritis and colitis, restoring epithelial integrity and mitochondrial function in bowel inflammation.

Research Gaps, Limitations, and Future Directions

Although preclinical data indicate that methylene blue has multi-target immunometabolic actions, the evidence base for its use in immune modulation is constrained by limited human trials, heterogeneous dosing, and incomplete mechanistic understanding. Human evidence remains sparse, with small, uncontrolled studies and variable formulations obscuring the detection of signals and safety boundaries.

Core molecular pathways—STAT3, IL-6 dynamics, mitochondrial redox cycling, and neutrophil/macrophage functional modulation—require time-resolved, cell-specific dissection to elucidate causality and dose-response relationships.

Prioritise randomised, dose-ranging trials with standardised purity, route comparisons, and pharmacokinetic-pharmacodynamic linkage.
Define temporal kinetics of IL-6 reduction, STAT3 inhibition, and mitochondrial coupling to align biomarkers with clinical endpoints.
Establish validated biomarkers for target engagement and immune trajectory, enabling cross-trial comparability and therapeutic implications.
Quantify variability across patient strata (age, comorbidities, immunosuppression), including long-term safety under repeated exposure.
Conduct mechanistically anchored antiviral studies separating virucidal effects from host-directed immunomodulation across pathogens.

Quality control, impurity profiling, and harmonised manufacturing standards are essential prerequisites for reproducibility and protocol generalisation.

Frequently Asked Questions

Can Methylene Blue Interact With Common Supplements or Herbal Products?

Yes. Evidence suggests significant interactions between methylene blue and herbal supplements and nutrients.

As an MAO inhibitor, it can synergise with St. John’s wort, 5-HTP, tryptophan, SAM-e, rhodiola, and kanna, elevating the risk of serotonin syndrome.

CNS effects may be augmented by kava, passion flower, and ashwagandha.

In G6PD deficiency, the risk of hemolysis increases.

Antioxidants (such as glutathione, alpha-lipoic acid, and CoQ10) and NAD+ precursors may modulate redox/mitochondrial actions.

Hawthorn, ginkgo, garlic, iron, and B vitamins warrant monitoring.

Are There Genetic Factors Affecting Individual Response to Methylene Blue?

Yes. Genetic polymorphisms modulate methylene blue response via enzyme function and drug–gene interactions.

G6PD deficiency predisposes to hemolysis, especially at higher doses.

MAOA variants influence MAO-A inhibition sensitivity, affecting serotonin toxicity risk with SSRIs or MAOIs and potential mood effects.

Evidence also shows altered individual metabolism and mitochondrial gene expression responses, including downregulation of respiratory complex genes and Nrf2/ARE activation.

Clinical protocols require genotype screening, dose adjustments, and avoidance in pregnancy and nursing.

How Quickly Do Users Typically Notice Symptomatic Improvements?

Like a dimmer turning up, symptomatic relief is often reported within 24 to 72 hours.

User experiences align with trial data, showing early improvements in oxygen saturation and respiratory rate by day 3, with sustained gains by day 5.

Mechanistically, effects likely stem from enhanced cellular redox cycling, mitochondrial support, and antiviral actions.

Variability occurs due to dose, co-therapies (such as vitamin C and NAC), and disease severity.

Some users report reductions in hospital stays and mortality benefits in controlled settings.

What Storage Conditions Preserve the Stability and Potency of Methylene Blue?

Methylene blue retains stability and potency when stored at room temperature in a calm, dry environment, reflecting temperature sensitivity below decomposition thresholds.

Tightly closed, well-sealed containers limit moisture ingress and contamination. Protection from light exposure prevents photodegradation; opaque or amber packaging is preferred.

Segregation oxidisers, reducing agents, bases, dichromates, and alkali iodides avoid reactive degradation. Avoid freezing and heat sources.

Use well-ventilated storage and minimise dust by keeping containers closed when not in use.

Is Methylene Blue Permitted in Competitive Sports or Anti-Doping Regulations?

Like a compass pointing true north, the answer is: yes, methylene blue is currently permitted under WADA doping regulations.

Evidence indicates that it is not listed on the WADA Prohibited List; athletes must verify this annually, as revisions take effect on January 1.

Classification criteria encompass performance enhancement, health risk, and the spirit of sport. Absent Scategorization, it remains permitted, although sport federations may impose stricter rules.

Athletes should confirm via GlobalDRO and their governing body’s advisories.

Conclusion

In summary, methylene blue modulates inflammation through redox cycling, attenuation of the NF-κB/MAPK pathway, normalisation of cytokines, and mitochondrial rescue, with additional effects on antioxidants and immune cell function.

Evidence spans in vitro, animal models, and limited clinical data, with cautious dosing due to risks associated with AOI activity and G6PD deficiency.

Consider a hypothetical ICU patient with COVID-19 cytokine storm and mitochondrial dysfunction. Low-dose methylene blue adjunctively reduces IL-6/TNF-α, restores complex IV flux, and improves vasoplegia; however, it necessitates monitoring for serotonin toxicity and careful pharmacovigilance, as per randomised, controlled validation.

Methylene Blue and the Immune System: Mechanisms, Evidence, and Considerations

Key Takeaways

Anti-Inflammatory Mechanisms and Immune Modulation

Cytokine Regulation and Inflammatory Signalling Pathways

Mitochondrial Protection and Cellular Energy Support