Cyclooxygenase-2

Studies report arctigenin as the most potent bioactive component of A. lappa; in vitro and preclinical data indicate modulation of NF-κB signalling, suppression of TNF-α and IL-6, and inhibition of COX-2/PGE2 pathways. AMPK activation has also been reported in preclinical models.

Arctiin is the glycosidic precursor to arctigenin; studies report anti-inflammatory activity including inhibition of cytokine induction (IL-6, TNF-α) and downstream NF-κB signalling. In vitro data also suggest collagen-stimulating activity relevant to dermal matrix remodelling.

Flavonoids identified in A. lappa; preclinical data link these compounds to COX-2 and NF-κB modulation.

Preclinical studies report NF-κB pathway and COX-2 modulation; xanthine oxidase inhibitory activity investigated in vitro (Zhang et al. 2018; Annaz et al. 2022)

In vitro evidence suggests AMPK activation and PPAR-γ agonism relevant to metabolic contexts; anti-inflammatory activity via NF-κB and COX pathways reported in preclinical models (Zhang et al. 2018)

Preclinical anti-inflammatory activity reported; contribution to whole-plant effects in human studies unclear (Annaz et al. 2022)

Identified in vitro as a principal active constituent responsible for cyclooxygenase and 5-lipoxygenase inhibitory activity in n-hexane extracts; content correlated with inhibitory potency across commercial samples (Zschocke et al., 1997).

Reported in vitro to inhibit 5-lipoxygenase and cyclooxygenase (Zschocke et al., 1997); additionally reported to activate Nrf2/ARE pathway, inducing antioxidant and phase-2 drug-metabolizing enzymes in cultured hepatic cells (Ohnuma et al., 2009); also demonstrated partial PPARγ agonism in reporter assays (Atanasov et al., 2013).

Identified as a minor active constituent contributing to cyclooxygenase and 5-lipoxygenase inhibition in vitro (Zschocke et al., 1997).

Broader pharmacological literature proposes inhibition of NF-κB pathway activation and COX-2 expression in vitro; these specific targets are not named in the cited abstracts. Clinical relevance is not established.

Broader review literature proposes antioxidant and anti-inflammatory activity via NF-κB and COX-2 inhibition in vitro; these specific targets are not named in the cited abstracts. Clinical relevance is not established.

The al-Sereiti et al. (1999) review — one of the cited papers — reports that rosmarinic acid modulates prostaglandin E2 and leukotriene B4 production and inhibits the complement system. MAO inhibitory and COX-specific inhibitory designations are drawn from the broader pharmacological literature and are not directly described in the cited abstracts; clinical translation is not established.

Preclinical studies report inhibition of NF-κB signalling and cyclooxygenase pathways; also investigated for antimicrobial activity against Gram-positive bacteria and fungi in vitro.

Found in highest concentrations in cashew nut shell liquid (CNSL); reported antioxidant activity in preclinical models.

Co-present with cardanols in CNSL; preclinical anti-inflammatory activity reported.

Piperine is reported in preclinical studies to activate TRPV1, inhibit COX and LOX pathways, suppress NF-κB signalling, and modulate serotonin reuptake. Bioavailability-enhancement properties (inhibition of drug-metabolising enzymes including CYP3A4 and P-gp) are extensively discussed in systematic review data (Takooree et al. 2019).

Preclinical data reviewed in Yadav et al. 2020 report anti-inflammatory and antiproliferative activity ascribed in part to NF-κB and eicosanoid pathway modulation.

Preclinical studies report inhibition of NF-κB signalling and downstream inflammatory mediators; antioxidant activity attributed in part to free-radical scavenging.

Reported in preclinical models to modulate NF-κB pathway and COX-2 expression; mechanism in thyroid tissue under investigation.

Preclinical reports describe inhibition of COX-2 and 5-LOX, suppression of NF-κB, and AMPK activation relevant to metabolic signalling (Zhao et al., 2019; Wang et al., 2018).

Preclinical data indicate anti-inflammatory activity via NF-κB and COX-2 inhibition (Wang et al., 2018).

Primary fresh-ginger constituents; broad eicosanoid modulation. 6-gingerol is the most abundant.

Form during drying/heating of ginger; more potent NF-κB inhibition than parent gingerols.

Preclinical data cited in Shah et al. (2011) describe proposed anti-inflammatory activity via inhibition of NF-κB signalling and downstream mediators; direct clinical translation not established.

Flavonoid fraction reported in preclinical literature to modulate cyclooxygenase and NF-κB pathways; human pharmacokinetic data limited.

Methyl salicylate shares cyclooxygenase-inhibiting mechanism with salicylate class compounds; relevance at concentrations achieved from plant use is unclear.

Ursolic acid has been investigated for COX-2 and NF-κB inhibition in in-vitro and animal models; clinical translation unestablished.

In vitro studies report agrimoniin-enriched fractions inhibit COX-2 expression in HaCaT keratinocytes and modulate NF-κB signaling; described as a potent radical scavenger (citation [3]).

In silico binding affinity for COX-2 and related inflammatory targets reported for ellagic acid and chlorogenic acid in topical gel modelling (citation [6]).

In vitro and in vivo studies report that isothiocyanates (e.g., sulforaphane) may modulate NF-κB signalling, COX-2 expression, and TNF-α levels; indole-3-carbinol has been investigated for aromatase modulation. Evidence is largely preclinical.

Red cabbage anthocyanins demonstrate dose-dependent urinary bioavailability in human volunteers; preclinical studies associate them with anti-inflammatory pathway modulation. Clinical magnitude of effect is not established.

Safe et al. (2021) describe apigenin's interactions with COX-2 and NF-κB pathways in preclinical models; presence in V. officinalis is reported by Salehi et al. (2019) but clinical relevance for this species is unestablished.

Scutellarin is a flavone with reported preclinical anti-inflammatory activity via COX-2 and NF-κB modulation (Safe et al., 2021); identified in Veronica species by Salehi et al. (2019).

In vitro studies report inhibition of NF-κB signalling and downstream prostaglandin synthesis; clinical relevance in humans has not been established.

Preclinical data report modulation of pro-inflammatory cytokine pathways; human pharmacokinetic data are limited.

In vitro studies report flavonoid fractions from avocado leaves and pulp may inhibit NF-κB signalling, COX-2 expression, and TNF-α production (Bhuyan et al. 2019; Yasir et al. 2010)

Preclinical data indicate eugenol may inhibit COX-2 expression and NF-κB activation; investigated for anti-inflammatory and antimicrobial properties.

Flavonoids present in seed extracts have been investigated for anti-inflammatory pathway modulation in preclinical models

Review literature describes coptisine as exhibiting anti-inflammatory, anti-cancer, anti-bacterial, and cardioprotective activity in preclinical models, reportedly via NF-κB, COX-2, TNF-α, and IL-6 pathway modulation.

In vitro studies, reported in Wang et al. (2022) and Kulinowska et al. (2026), describe cytotoxic, antioxidant, and anti-inflammatory activities. Mechanistic in vivo or clinical translation has not been established.

In vitro studies report inhibition of LPS-stimulated macrophage NO production and COX-2-mediated prostaglandin synthesis.

Preclinical studies suggest inhibition of cyclooxygenase isoforms and NF-κB-mediated inflammatory signalling; clinical translation not yet established from provided citations.

Preclinical studies report eugenol inhibits COX-1/COX-2 and NF-κB signalling, suppresses PGE2 synthesis, and modulates TRPV1 and voltage-gated sodium channels; proposed as the primary driver of observed analgesic and anti-inflammatory signals.

Preclinical data suggest apigenin may modulate COX-2 expression and NF-κB signalling; reported anti-inflammatory activity in in vitro models. Clinical relevance in Plantago major preparations has not been directly confirmed.

Molecular docking and in vitro studies report binding to COX-2 active site and inhibition of inflammatory mediators; anti-inflammatory activity attributed in part to flavonoid fraction in rhizome extracts.

Standard flavonoid mechanisms investigated in vitro; COX-2 and PGE2 inhibition reported in cell-free and cell-based assays for these compound classes generally; attribution to G. robertianum extracts specifically requires further study.

Rosmarinic acid biosynthesis in A. rugosa has been characterised metabolomically; the compound class is broadly studied for antioxidant and anti-inflammatory mechanisms in preclinical models.

BITC, released from glucotropaeolin by gut bacterial myrosinase-like activity, has been investigated for antimicrobial and anti-inflammatory activity. Studies report modulation of NF-κB and COX-2 pathways in preclinical models; clinical relevance in humans is under investigation.

Apigenin is the principal flavone studied in parsley. In vitro and animal research has investigated inhibition of COX-2 and NF-κB inflammatory signalling, suppression of TNF-α, and aromatase (CYP19A1) inhibition. Human absorption following parsley intake was confirmed in a randomised crossover trial (Nielsen et al., 1999), though downstream target engagement was measured via oxidative-stress biomarkers rather than direct receptor assays.

Reviews describe inhibition of COX-2 and NF-κB and activation of AMPK in vitro; clinical relevance at consumed doses is unestablished.

Preclinical data report anti-inflammatory activity attributed in part to inhibition of COX-2 and suppression of NF-κB and TNF-α signalling pathways.

Beyond its anti-inflammatory NF-kB/COX/LOX activity, curcumin has been investigated in preclinical cancer models for EGFR-pathway and PI3K–Akt–mTOR signaling inhibition and for anti-angiogenic (VEGF) effects. Research only — not a treatment claim.

Preclinical and review literature reports modulation of NF-κB and COX-2 inflammatory pathways; direct clinical confirmation in humans remains limited.

Hepatically metabolized to salicylic acid — chemically the active metabolite of aspirin. The mechanism overlap with NSAIDs is therefore direct rather than analogous.

Preclinical studies report inhibition of NF-κB activation via suppression of IRAK1, TAK1, IKKβ, and IκBα phosphorylation in LPS-stimulated macrophages; associated with downstream reduction of inflammatory mediators in murine colitis models.

The genus name Spiraea (older botanical name) gave aspirin its name — Bayer's 1899 acetylsalicylic acid was developed from spiraein extracted from this plant. Salicylate-induced COX inhibition produces analgesic, anti-inflammatory, and antipyretic effects, weaker but mechanistically identical to aspirin.

Salicylic acid is a recognized COX pathway modulator; direct attribution of this activity to Iris versicolor preparations has not been established in verified clinical literature.