Effect of alisol B acetate, a plant triterpene, on apoptosis in vascular smooth muscle cells and lymphocytes

Add time:09/26/2019    Source:infona.pl

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 (IC 5 0 =4.0+/-0.8x10 - 6 M in A7r5 and 2.1+/-1.2x10 - 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 (ΔΨ 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.

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