Prostaglandin E2

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.

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

GLA is a precursor to dihomo-GLA (DGLA) and subsequently to prostaglandin E1 (PGE1); studies propose this downstream pathway may modulate prostaglandin and leukotriene synthesis. In vitro studies report DGLA-derived metabolites may competitively inhibit arachidonic-acid-derived pro-inflammatory eicosanoids via COX and 5-LOX pathways. Platelet-activating factor and thromboxane A2 pathway modulation has also been proposed mechanistically.

Partially converts to EPA and DHA; substrate for anti-inflammatory eicosanoid production (decreased PGE2 and TXA2 production), explaining cardiovascular and anti-inflammatory benefits.

The active laxative mechanism of senna is well documented: sennosides are activated by colonic bacteria to rhein-anthrone, which stimulates colonic secretion and motility in part through induction of prostaglandin E2 (and nitric oxide). PGE2-mediated fluid secretion is a documented, compound-specific component of the sennoside/rhein mechanism, not a generic anti-inflammatory attribution.

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

Inhibits NF-κB activation, reducing downstream TNF-α and prostaglandin E2 production; the principal anti-inflammatory and (in oral exposure) toxic constituent.

Converted to dihomo-γ-linolenic acid (DGLA), then to series-1 prostaglandins (PGE1) — anti-inflammatory eicosanoids. The metabolic pathway shifts the inflammation profile toward less inflammatory mediators, providing the basis for benefit in inflammatory arthritis and atopic conditions.

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.

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

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

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.

Anti-inflammatory and expectorant — irritates respiratory mucosa to stimulate ciliary clearance of mucus; the same chemistry underlies historical antimycobacterial use against tuberculosis (alantolactone shows activity against M. tuberculosis in vitro).

Anti-inflammatory and anti-lithiatic — reduces calcium oxalate stone formation in animal models. Smooth-muscle relaxant on bladder and ureter, supporting traditional use in BPH and urinary calculi.