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DOI: 10.1055/s-0028-1083991
Boswellic acids from the anti-inflammatory remedy frankincense: Identification and functional analysis of novel molecular targets within the arachidonic acid cascacde
Boswellic acids (BAs) are pharmacologically active principles from frankincense that is traditionally applied in the treatment of inflammatory disorders. Initially, BAs were found to block the formation of leukotrienes by inhibiting 5-lipoxygenase (5-LO), whereas interference with platelet-type 12-lipoxygenase (p12-LO) and cyclooxygenases (COX) has been excluded [1]. Here, we provide evidence for a molecular interference of select BAs with COX-1 or 12p-LO. We show that 11-keto-β-BAs concentration-dependently inhibit COX-1 and p12-LO product formation in stimulated human platelets (IC50=6–17µM) and in cell-free assays [2, 3]. The inhibitory effect of BAs on COX-1 is reversible, and increasing the arachidonic acid concentration impairs the efficacy. In a protein fishing assay, both COX-1 and p12-LO from platelet lysates selectively bound to a BA-affinity matrix. Also isolated COX-1 enzyme bound to the immobilized BAs and this binding was reversed by ibuprofen or arachidonic acid. Automated molecular docking of BAs into X-ray structures of COX-1 indicate favorable binding to the active site of the enzyme. In contrast, COX-2 was hardly inhibited by BAs. To improve the potency of BAs, structural derivatives were designed and synthesized. Structure-activity-relationship studies revealed potent BA-derivatives with submicromolar IC50 values for both COX-1 and p12-LO. In conclusion, BAs directly interfere with COX-1 and p12-LO and may mediate their anti-inflammatory actions not only by suppression of 5-LO, but also by inhibiting COX-1 and p12-LO. These findings underline the anti-inflammatory effectiveness of frankincense extracts on one hand, but also may unravel novel therapeutic indications for pharmacological intervention using frankincense.
Acknowledgements: Deutsche Forschungsgemeinschaft and Pharmasan GmbH, Germany.
References: 1. Safayhi et al. (1992)J Phramacol Exp Ther 261:1143–6
2. Siemoneit et al. (2008) Biochem Pharmacol 75:503–13
3. Poeckel et al. (2006) Mol Pharmacol 70:1071–8