From the CH(2)Cl(2) extract of the sponge Hyrtios cf. erecta, collected from Fiji, two new sesterterpenes, 1 and 2, and the known compounds isodehydroluffariellolide (3), homofascaplysin A (4), and fascaplysin (5) were isolated. The structures of 1-5 were established employing 1D and 2D NMR spectroscopy and mass spectrometry. All NMR resonances of fascaplysin (5) have been unambiguously assigned. Evaluation of the biological activity of the extracts and pure compounds toward Plasmodium falciparum, Trypanosoma brucei subsp. rhodesiense, Trypanosoma cruzi, hepatitis A virus (HAV), several other microbial targets, and HIV-1-RT and p56(lck) tyrosine kinase revealed new activities for homofascaplysin (4) and fascaplysin (5), both being potently active in vitro against P. falciparum.

Melittin can induce apoptosis of human gastric cancer (GC) cells through the mitochondria pathways, and it may be a potent agent in the treatment of human GC.

No abstract

Apigenin is a naturally occurring plant flavonoid that possesses antioxidant, anti-cancer and anti-inflammatory properties. However, there are few reports has been done on the ability of apigenin to induce apoptosis in macrophages. In this study, mouse macrophage ANA-1 cells were incubated with different concentrations of apigenin. The cell viability was determined by an MTT assay. The cell apoptosis were analyzed by flow cytometric analysis. Apoptosis were also analyzed using a TUNEL assay and a DNA ladder. The level of intracellular ROS was detected using a dichlorofluorescein -diacetate probe. The expression levels of apoptosis-related proteins were detected by western blot analysis. The results showed that apigenin decreased the viability of ANA-1 cells and induced apoptosis in a dose- and time-dependent manner. Apigenin increased the level of intracellular ROS, downregulated the expression of Bcl-2 and upregulated the expression of caspase-3 and caspase-8 in ANA-1 cells. Furthermore, apigenin downregulated the expression of phospho-ERK and phospho-JNK, upregulated the expression of phospho-p38 and had no significant effect on the expression of Bax, ERK, JNK and p38. The results suggested that apigenin induced cell apoptosis in mouse macrophage ANA-1 cells may via increasing intracellular ROS, regulating the MAPK pathway, and then inhibiting Bcl-2 expression.

No abstract