No abstract

Traditional Chinese herbs are regarded as a new and promising source of potential anti-cancer remedies and new chemotherapy adjuvants to enhance the efficacy of chemotherapy and/or to ameliorate its side effects. Extensive investigations have been undertaken both in the experimental and clinical studies over the years to augment the efficacy of chemotherapy. Evodia rutaecarpa is a very popular multi-purpose herb traditionally used in China for the treatment of headaches, abdominal pain, postpartum hemorrhage, dysentery and amenorrhea. The major constituents of Evodia rutaecarpa are evodiamine and rutaecarpine. Growing evidence demonstrates that evodiamine possesses anti-cancer activities both in vitro and in vivo by inhibiting proliferation, invasion and metastasis, inducing apoptosis of a variety of tumor cell lines. This review is aimed to summarize the recent researches on evodiamine focusing on anti-cancer activity and to highlight molecular mechanisms during the past ten years.

Objective-Vascular endothelial growth factor (VEGF), a key angiogenic growth factor, stimulates angiogenesis. Low levels of reactive oxygen species (ROS) function as signaling molecules for angiogenesis. We postulated that low concentrations of oxLDL might induce low levels of ROS and initiate angiogenesis. Methods and Results-An in vitro model of tube formation from human coronary artery endothelial cells (HCAECs) was used.oxLDL (0.1, 1, 2, 5 g/mL) induced VEGF expression and enhanced tube formation. oxLDL-mediated VEGF expression and tube formation were suppressed by a specific blocking anti-LOX-1 antibody. Anti-LOX-1 antibody also reduced oxLDL-induced increase in the expression of NADPH oxidase (gp91 phox and p47 phox subunits) and subsequent intracellular ROS generation, phosphorylation of p38 as well as p44/42MAPK, and NF-B p65 expression. gp91 phox siRNA had a similar effect. The expression of VEGF and NF-B p65 induced by oxLDL was also inhibited by the specific extracellular signal-regulated kinase (ERK) 1/2 inhibitor U0126 and the p38 MAPK inhibitor SB203580. Importantly, the NADPH oxidase inhibitor apocynin, gp91 phox siRNA, U0126, and SB203580 all reduced tube formation in response to oxLDL. Conclusions-These