title: Effect of alisol B acetate, a plant triterpene, on apoptosis in vascular smooth muscle cells and lymphocytes.
abstract: Glucocorticoid-induced apoptosis is a well-recognized physiological regulator of T-cell number and function. Alisol B acetate, a triterpene from Alisma Plantago-aquatica, has a glucocorticoid-like structure, and may have a similar function like glucocorticoid-induced apoptosis in both vascular smooth muscle cell line (A7r5) and human acute lymphoblastic leukemia cell line (CEM cells). For exploring its mechanism, mitochondria membrane potential and apoptosis-related gene expression were discussed. Alisol B (10(-6)-10(-4) M) inhibited serum-stimulated DNA synthesis in a concentration-dependent manner (IC50) = 4.0 +/- 0.8 x 10(-6) M in A7r5 and 2.1 +/- 1.2 x 10(-6) M in CEM cells). The cell viability was reduced at 10(-4) M of alisol B. Similar results were seen in dexamethasone treatment (a synthetic glucocorticoid, 10(-6) M, 48 h). Apoptosis was induced after the cells were exposed to 10(-5)-10(-4) M alisol B or 10(-6) M dexamethasone for 48 h. The mitochondrial membrane potential (delta psi(m)) was significantly reduced after the alisol B treatment, indicating that the mitochondria might play a role in the alisol B induced cell apoptosis. Alisol B (10(-5)-10(-4) M) increased the levels of c-myc and bax mRNA and proteins, but not on the anti-apoptotic proto-oncogene, bcl-2, in A7r5 and CEM cells. In contrast, dexamethasone (10(-6) M) treatment only caused significant increase in c-myc mRNA levels. These results suggest that the increased ratio of Bax/Bcl-2 and the decreased mitochondrial membrane potential might be involved in the mechanisms of alisol B-induced cell apoptosis.
authors: Office for Medical Research, National Taiwan University Hospital, Taipei.
authors: H W
authors: HW
authors: Chen
authors: M J
authors: MJ
authors: Hsu
authors: C T
authors: CT
authors: Chien
authors: H C
authors: HC
authors: Huang
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D002783:Cholestenones / Q000494:pharmacology*; D004247:DNA / Q000096:biosynthesis*; D003907:Dexamethasone / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005434:Flow Cytometry; D016259:Genes, myc / Q000187:drug effects*; D006801:Humans; D020287:In Situ Nick-End Labeling; D008214:Lymphocytes / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D016133:Polymerase Chain Reaction; D000090063:Proto-Oncogene Mas; D051381:Rats; D014407:Tumor Cells, Cultured / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D002783:Cholestenones; D004791:Enzyme Inhibitors; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; C401295:alisol B monoacetate; D003907:Dexamethasone; D004247:DNA