%0 Journal Article
%T The Medicinal Timber Canarium patentinervium Miq. (Burseraceae Kunth.) Is an Anti-Inflammatory Bioresource of Dual Inhibitors of Cyclooxygenase (COX) and 5-Lipoxygenase (5-LOX)
%A R. Mogana
%A K. Teng-Jin
%A C. Wiart
%J ISRN Biotechnology
%D 2013
%R 10.5402/2013/986361
%X The barks and leaves extracts of Canarium patentinervium Miq. (Burseraceae Kunth.) were investigated for cyclooxygenase (COX) and 5-lipoxygenase (LOX) inhibition via in vitro models. The corresponding antioxidative power of the plant extract was also tested via nonenzyme and enzyme in vitro assays. The ethanolic extract of leaves inhibited the enzymatic activity of 5-LOX, COX-1, and COX-2 with IC50 equal to £¿¦Ìg/mL, £¿¦Ìg/mL, and £¿¦Ìg/mL, respectively, with selective COX-2 activity noted in ethanolic extract of barks with COX-1/COX-2 ratio of 1.22. The ethanol extract of barks confronted oxidation in the ABTS, DPPH, and FRAP assay with EC50 values equal to £¿¦Ìg/mL, £¿¦Ìg/mL, and £¿¦Ìg/mL, respectively, while the ethanol extract of leaves confronted oxidation in ¦Â-carotene bleaching assay and superoxide dismutase (SOD) assay with EC50 value of £¿¦Ìg/mL and IC50 value of £¿¦Ìg/mL. The ethanol extract acts as a dual inhibitor of LOX and COX enzymes with potent antioxidant capacity. The clinical significance of these data is quite clear that they support a role for Canarium patentinervium Miq. (Burseraceae Kunth.) as a source of lead compounds in the management of inflammatory diseases. 1. Introduction Inflammation is a physiological response process that is generated by the body in the event of oxidative stress, injury, infection, or irritation. Chronic inflammation involves the release of a number of mediators, resulting in the proliferation of fibroblasts and vascular endothelium, as well as lymphocytes, plasma cells, and macrophages [1]. The release of all these mediators can contribute to chronic degenerative diseases such as arthritis, cancer, heart disease, Alzheimer¡¯s disease, diabetes, and asthma, which may increase disease-associated morbidity. Inflammation in injured cells is both initiated and maintained by the overproduction of prostaglandins and leukotrienes, which are produced by separate enzymatic pathways, namely, the cyclooxygenase (COX) and lipoxygenase (LOX) pathways, respectively. Both the prostaglandins as well as the leukotrienes are on demand biosynthesised from arachidonic acid (AA), which is a 20-carbon fatty acid, derived from the breakdown of cell membrane phospholipids by any number of phospholipase A2 (PLA2) isoforms. AA is then further metabolized by the COX and 5-LOX enzyme systems to a variety of mediator molecules, including prostaglandin (PG) E2, thromboxanes (TXs) (TXA2), prostacyclins (PGI2), and highly inflammatory leukotrienes such as leukotriene (LT) B4, LTC4, and LTD4. Conventional pharmacological management of inflammatory
%U http://www.hindawi.com/journals/isrn.biotechnology/2013/986361/