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 × 10-6 M in A7r5 and 2.1 ± 1.2 × 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 (ΔΨm) 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.
- A7r5 vascular smooth muscle cell
- Alisol B acetate
- CEM lymphocyte
- Mitochondria membrane potential
ASJC Scopus subject areas