Effects of total flavonoids from Dracocephalum moldavica on the proliferation, migration, and adhesion molecule expression of rat vascular smooth muscle cells induced by TNF-α.

BACKGROUND

Dracocephalum moldavica Linn (Labiatae) is one of the ethnomedicinal drugs of Uygur in Xinjiang, China. This herb is mainly used in treating cardiovascular diseases, such as atherosclerosis. However, the mechanism of pharmacological activity of D. moldavica has been poorly studied.

OBJECTIVE

To explore the pharmacological mechanism of D. moldavica in treating atherosclerosis by investigating the effects of total flavonoids from the aerial portion of D. moldavica on rat vascular smooth muscle cells (VSMCs).

METHODS

The proliferation and migration of VSMCs were evaluated via a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and transwell chamber experiment, respectively. The expression of proliferating cell nuclear antigen (PCNA), nuclear factor κB p65 (NF-κB p65), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) of VSMCs was determined using immunohistochemistry staining and quantitative real-time PCR (qRT-PCR).

RESULTS

Total flavonoids (IC(50) = 145.63 μg/mL) significantly inhibited tumor necrosis factor-α (TNF-α) induced VSMC proliferation at concentrations of 25, 50, and 100 μg/mL. Treatment with 50 and 100 μg/mL of total flavonoids also significantly inhibited TNF-α-induced VSMC migration, whereas 25 μg/mL of total flavonoids did not elicit any significant inhibitory effect. In addition, the effects of total flavonoids on inflammatory molecule expression of cells were tested by immunohistochemistry staining, showing that TNF-α-induced expression of PCNA, NF-κB p65, ICAM-1, and VCAM-1 in VSMCs was dose-dependently suppressed by total flavonoids. Furthermore, qRT-PCR data confirmed the inhibition of mRNA expressions of these inflammatory molecules.

CONCLUSIONS

These data suggest that total flavonoids from D. moldavica exhibit anti-inflammatory activities, which is probably one of the underlying mechanisms of D. moldavica for clinical treatment of atherosclerosis.