Abstract
Purpose: To investigate the antioxidant, anti-inflammatory, antidiabetic, cardiovascular and cytotoxic activities of the leaf extract and major compounds isolated from Abelia triflora R. Br. (Caprifoliaceae)
Methods: The chloroform soluble fraction of A. triflora leaves was subjected to several column chromatographic separations to isolate its constituents. Anti-inflammatory and antioxidant activities were determined in terms of the ability to inhibit NF-kB, iNOS activity and lipoxygenase enzyme, and to decrease oxidative stress in HepG2 cells. Antidiabetic and cardiovascular activities were determined by screening for peroxisome proliferator-activated receptor alpha (PPARa) and PPAR. agonistic activities. In vitro cytotoxic activity was determined against a set of four human cancer cell lines (SK-MEL, KB, BT-549, SK-OV-3) and two non-cancerous kidney cell lines (LLC-PK1 and VERO). Cell viability was measured by neutral red assay.
Results: Three triterpene acids were isolated from the chloroform fraction namely; ursolic acid (4), 2, 3-dihydroxy ursolic acid (5) and 2, 3, 21-trihydroxy ursolic acid (6). The results showed that ursolic acid exhibited potent inhibition of lipoxygenase enzyme and iNOS (inducible nitric oxide synthase) activity with IC50 (half-maximal inhibitory concentration) value of 13.0 mu g/mL, compared to parthenolide positive standard (IC50, 0.3 mu g/mL); furthermore, it inhibited NF-kB (nuclear factor-kappa B) with IC50 of 25.0 mu g/mL, compared to parthenolide (positive standard, (IC50, 0.5 mu g/mL). Also, ursolic acid possessed the highest cytotoxic effect against the three cell lines, SK-MEL (IC50, 14.5 mu g/mL), BT-549 (IC50, 16.0 mu g/mL) and SK-OV-3 (IC50, 12.5 mu g/mL). Only 2,3-dihydroxy ursolic acid activated PPAR. (1.5-fold at 25 mu M), compared to rosiglitazone (positive standard, 3.7 fold at 10 mu M)
Conclusion: Among the investigated compounds, ursolic acid exhibited the highest anti-inflammatory and cytotoxic activities, while 2,3-dihydroxy ursolic acid demonstrated antidiabetic activity via activation of PPAR gamma.