Apoptosis rosemary

Camosol (Figure 4), a phenolic antioxidant extracted from the herb rosemary, exhibits anticancer activity in animal model for both breast and skin tumorigenesis (68,69). Camosol induced apoptosis accompanied by a dismption of the mitochondrial membrane potential (70). Further analysis revealed that camosol treatment down-regulated the anti-apoptotic protein Bcl-2 in leukemia cell lines and this reduction of Bcl-2 may contribute to the apoptotic effects of cmiosol. Recently we demonstrated that camosol suppresses inducible nitric oxide synthase through down-regulating NFkB in mouse macrophages (77). 

The aim of this study is to elucidate whether camosic acid, camosol, rosmarinic acid and ursolic acid have any effects on apoptotic induction, since ursolic acid was previously reported to possess this effect previously (28). We used HL-60 cells to investigate the molecular mechanisms involved. We examined the effects of these rosemary phytochemicals on DNA fragmentation, activation of caspases, altering the mitochondrial function, ROS generation and releasing of cytochrome c from mitochondria. In the present study, we have demonstrated camosic acid, camosol, and ursolic acid induced apoptosis in HL-60 ceils and activated caspase-3 and caspase-9 via provoking the release of cytochrome c. 

---