In this study, 221 phytocompounds were evaluated for activity against anti-severe acute respiratory syndrome associated coronavirus (SARS-CoV) activities using a cell-based assay measuring SARS-CoV-induced cytopathogenic effect on Vero E6 cells. Ten diterpenoids (1-10), two sesquiterpenoids (11 and 12), two triterpenoids (13 and 14), five lignoids (15-19), curcumin (20), and reference controls niclosamide (21) and valinomycin (22) were potent inhibitors at concentrations between 3.3 and 10 µM. The concentrations of the 22 compounds to inhibit 50% of Vero E6 cell proliferation (CC 50 ) and viral replication (EC 50 ) were measured. The selective index values (SI ) CC 50 /EC 50 ) of the most potent compounds 1, 5, 6, 8, 14, and 16 were 58, >510, 111, 193, 180, and >667, respectively. Betulinic acid (13) and savinin (16) were competitive inhibitors of SARS-CoV 3CL protease with K i values ) 8.2 ( 0.7 and 9.1 ( 2.4 µM, respectively. Our findings suggest that specific abietane-type diterpenoids and lignoids exhibit strong anti-SARS-CoV effects.

The antioxidant activity of extracts from bark and heartwood of Acacia confusa was evaluated by various antioxidant assays, including free radical and superoxide radical scavenging assays and lipid peroxidation assay as well as hydroxyl radical-induced DNA strand scission assay. In addition, an ex vivo antioxidant assay using a flow cytometric technique was also employed in this study. The results indicate that both bark and heartwood extracts clearly have strong antioxidant effects. Similar inhibitory activities for each test sample were found for both 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical generation and lipid peroxidation. As for the superoxide radical scavenging activity, the heartwood extract was more effective than the bark extract. Furthermore, the heartwood extract protected PhiX174 supercoiled DNA against strand scission induced by ultraviolet photolysis of H2O2, and it reduced the amounts of intracellular hydrogen peroxide, a reactive oxygen species, when it was co-incubated with human promyelocytic leukemia (HL-60) cells under oxidative stress.

No abstract

No abstract

No abstract

1 Ethyl caffeate, a natural phenolic compound, was isolated from Bidens pilosa, a medicinal plant popularly used for treating certain inflammatory syndromes. The purpose of this study was to investigate the structural activity, and the anti-inflammatory functions and mechanism(s) of ethyl caffeate. 2 Ethyl caffeate was found to markedly suppress the lipopolysaccharide (LPS)-induced nitric oxide (NO) production (IC 50 ¼ 5.5 mg ml À1 ), mRNA and protein expressions of inducible nitric oxide synthase (iNOS), and prostaglandin E 2 (PGE 2 ) production in RAW 264.7 macrophages. 3 Transient gene expression assays using human cox-2 promoter construct revealed that ethyl caffeate exerted an inhibitory effect on cox-2 transcriptional activity in 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated MCF-7 cells. 4 Immunohistochemical studies of mouse skin demonstrated that TPA-induced COX-2 expression was significantly inhibited by ethyl caffeate with a superior effect to that of celecoxib, a nonsteroidal anti-inflammatory drug. 5 The phosphorylation and degradation of inhibitor kB (IkB) and the translocation of nuclear transcription factor-kB (NF-kB) into the nucleus, as well as the activation of mitogen-activated protein kinases (MAPKs) induced by LPS in macrophages, were not affected by ethyl caffeate. Ethyl caffeate, however, could inhibit NF-kB activation by impairing the binding of NF-kB to its cis-acting element. These results suggest that ethyl caffeate suppresses iNOS and COX-2 expressions partly through the inhibition of the NF-kB Á DNA complex formation. 6 Structure-activity relationship analyses suggested that the catechol moiety and a,b-unsaturated ester group in ethyl caffeate are important and essential structural features for preventing NFkB Á DNA complex formation. This study provides an insight into the probable mechanism(s) underlying the anti-inflammatory and therapeutic properties of ethyl caffeate.

No abstract

No abstract