A new isoflavonoid, excelsanone (2), was isolated from the ethyl acetate extract of Erythrina excelsa Backer stem bark, together with three known compounds namely 6,8diprenylgenistein (3), β-sitosterol (1) and sitosteryl-β-D-glucopyranoside (4). Their structures were elucidated using spectroscopic methods (HR-ESI-MS, NMR and IR) and by comparison with some data reported in literature. The antioxidant activity of crude extracts and two isolated compounds was evaluated using free radical scavenging (DPPH) and Ferric Reducing Ability Power (FRAP) methods with catechin as standard. The results of this radical scavenging activity showed that excelsanone (2) has a moderate potential with an IC 50 of 1.31 mg/ml. The cytotoxicity of compounds 2 and 3 as well as the ethyl acetate extract was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in two prostate cancer cell lines (DU145 and PC3). Excelsanone (2) induced a greater cytotoxicity in all tested cell lines, with a significant inhibition of DU145 cells growth in a concentration-dependent manner.

The endothelial cells’ dysfunction linked to the development of atherosclerosis plays an important role in the regulation of inflammatory responses. Previous studies demonstrated the antiatherogenic effects of Garcinia kola seed extracts based on their lipid lowering effects. Our recent studies showed the in vitro antioxidant and anti-inflammatory activities of the ethanolic extract of Garcinia kola stem barks (EE). For more insight on the antiatherogenic effect of EE, we investigated its activity on some key points of the atherosclerosis process. The cytotoxicity of EE as well as its effects on LDL-uptake, LPS-induced InterCellular Adhesion Molecule (ICAM-1) and Annexin-1 (Anxa-1) expression and LPS-induced DNA damage were evaluated in Human Umbilical Vein Endothelial Cells (HUVECs). EE significantly (p<0.0001) increased the cell viability in both naive and LPS-treated HUVECs. At the concentrations of 50 and 100 µg/ml, EE significantly reduced LDL-uptake by endothelial cells stimulated with LPS. The immunohistochemistry results showed a significant (p<0.01) decrease in the ICAM-1 expression at the EE concentration of 250 µg/ml. EE also showed a significant (p<0.0001) concentration-dependent reduction of Annexin-1 expression in LPS-treated HUVECs. Besides, EE exhibited significant inhibition on LPS-induced genotoxicity marked by a decrease in tail DNA expression (p<0.0001) and tail movement expression (p<0.001) for the concentrations of 50 and 100 µg/ml. These findings showed that EE may mitigate the atherogenic process by reducing LDL-uptake and the expression of adhesion molecules. Thus, the EE of Garcinia kola turns out to be a potential candidate for the treatment of atherosclerosis with a lower risk of toxicity. Keywords: Garcinia kola, LDL-uptake, LPS-induced inflammation, comet assay.

Psychotria densinervia hydro-ethanolic leaf extract (PHELE) and bark extract (PHEBE) were evaluated for antioxidant, anti-inflammatory, and inhibition of digestive enzymes activities. The antioxidant activity was characterized by 2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), ferric reducing antioxidant power (FRAP), total phenolic content (TPC), and total flavonoid content (TFC) assays. The anti-inflammatory activity was characterized by protein denaturation and antiproteinase tests, while the inhibition of the enzymes was assessed using α-amylase, α-glucosidase, lipase, and cholesterol esterase activities. PHELE presented low ( p < 0.001 ) IC50 (59.09 ± 5.97 μg/ml) for DPPH compared with ascorbic acid (71.78 ± 6.37 μg/ml) and PHEBE (115.40 ± 1.21 μg/ml). The IC50 of PHELE (262.4 ± 4.46 μg/ml) and PHEBE (354.2 ± 1.97 μg/ml) was higher ( p < 0.001 ) than that of catechin (33.48 ± 2.02 μg/ml) for ABTS. PHELE had high ( p < 0.001 ) FRAP (341.73 ± 21.70 mg CE/g) than PHEBE (150.30 ± 0.32 mg CE/g). PHELE presented ( p < 0.001 ) high TPC (270.05 ± 7.53 mg CE/g) and TFC (23.43 ± 0.032 mg CE/g) than PHEBE (TPC: 138.89 ± 0.91 and TFC: 20.06 ± 0.032 mg CE/g). PHELE showed antiprotein denaturation with IC50 (257.0 ± 7.51 μg/ml) ( p < 0.001 ) and antiproteinase activity (74.37 ± 1.10 μg/ml) lower than PHEBE (316.1 ± 6.02 μg/ml and 177.6 ± 0.50 μg/ml), respectively. Orlistat inhibited lipase ( p < 0.001 ) activity with IC50 (37.11 ± 4.39 μg/ml) lower than PHELE and PHEBE (50.57 ± 2.89 μg/ml and 62.88 ± 1.74 μg/ml, respectively). PHELE inhibited cholesterol esterase with IC50 (34.75 ± 3.87 μg/ml) lower than orlistat (54.61 ± 2.56) and PHEBE (80.14 ± 1.71 μg/ml). PHELE inhibited α-amylase IC50 (6.07 ± 4.05 μg/ml) lower than PHEBE (19.69 ± 6.27 μg/ml) and acarbose (20.01 ± 2.84 μg/ml). Acarbose inhibited α-glucosidase ( p < 0.001 ) activity with IC50 (4.11 ± 3.47 μg/ml) lower than PHELE (24.41 ± 2.84 μg/ml) and PHEBE (38.81 ± 2.46 μg/ml). PHELE presented better antioxidant, anti-inflammatory, and enzyme inhibition activity than PHEBE.