In an erythroleukemic cell line, beta-elemene inhibited telomerase activity, which was enhanced in combination with cyclophosphamide (9). It also demonstrated anti-fibrotic effects, inducing decreases in plasma angiotensin II levels and angiotensin II receptor type 1 expression, reducing collagen formation in a liver fibrosis rat model (10). Beta-elemene also exhibits anti-inflammatory effects, with reduction in LPS-induced nitric oxide production and prostaglandin E2 by rat peritoneal macrophages (11).
Beta-elemene has been shown to affect cancer cells via different mechanisms. In an in vitro study, following administration of beta-elemene, leukemia cells were arrested in S/G2 phase and underwent apoptosis (2). The antiproliferative effects were dependent on p38 MAPK activation/phosphorylation, cell cycle arrest in G0/G1, and inhibition of tumor growth of glioblastoma cells (3). Beta-elemene also induced G2/M arrest in lung carcinoma cells and ovarian cancer cells by combined reduction of cell-cycle promoters Cdc2 and cyclin B1, and elevated cell cycle regulators p53 and p27 (4) (5). Derivatives of beta-elemene showed antiproliferative activity in human cervical carcinoma cells through a decrease in cell cycle protein Cyclin D1 and thus cell cycle suppression (14). Furthermore, beta-elemene may enhance the effects of chemotherapy and radiation. In non-small cell lung cancer cells, apoptosis was induced by increased expression of Bax and p-Bcl-2, decreased Bcl-2 and XIAP, and augmented cisplatin-induced increases in caspase activity (6). In another study, apoptosis response to the taxanes paclitaxel and docetaxel in lung carcinoma cells was enhanced with beta-elemene, through increases in cytochrome c, caspase activity, downregulation of Bcl-2, and altered cell membrane permeability (7). Beta-elemene combined with radiation induced apoptosis in lung adenocarcinoma cells, possibly by sensitizing cancer cells to radiation (8).