Mechanism of Action

Animal studies performed in India showed ingestion of a defatted alcoholic extract of Boswellia decreased polymorphonuclear leukocyte infiltration and migration, decreased primary antibody synthesis,1,2 and caused almost total inhibition of the classical complement pathway.3 In an in vitro study of the effects of beta-Boswellic acid on the complement system, the extract demonstrated a marked inhibitory effect on both the classical and alternate complement systems.4 An investigation of Boswellia's analgesic and psychopharmacologic effects noted that it "was found to exhibit marked sedative and analgesic effects" in these animals.5 In vitro testing revealed Boswellia specifically, and in a dose-dependent manner, blocks the synthesis of pro-inflammatory 5-lipoxygenase products, including 5-hydroxyeicosatetraenoic acid (5-HETE) and leukotriene B4 (LTB4),6 which cause bronchoconstriction, chemotaxis, and increased vascular permeability.7 Other anti-inflammatory plant constituents, such as quercetin, also block this enzyme, but they do so in a more general fashion, as an antioxidant; whereas, Boswellia seems to be a specific inhibitor of 5-lipoxygenase.8,9 Boswellia has also been observed to inhibit human leukocyte elastase (HLE), which may be involved in the pathogenesis of emphysema. HLE also stimulates mucus secretion and thus may play a role in cystic fibrosis, chronic bronchitis, and acute respiratory distress syndrome.10,11 It is known that non-steroidal anti-inflammatory drugs can cause a disruption of glycosaminoglycan synthesis which can accelerate the articular damage in arthritic conditions.12-15 A recent in vivo study examined Boswellia extract and ketoprofen for their effects on glycosaminoglycan metabolism. Boswellia significantly reduced the degradation of glycosaminoglycans compared to controls, whereas ketoprofen caused a reduction in total tissue glycosaminoglycan content.16