Objective To explore the underlying possible mechanism of delaying endothelial cells aging by the extracts from Renshen（ Panax ginseng

人参）

Sanqi（ Panax notoginseng

三七） and Chuanxiong（ Ligusticum wallichii

川芎）（ Ext）. Methods By in vitro method for cell passage

the replicate senescent model of endothelial cells was established by human cardiac microvascular endothelial cells（ HCMEC） developing into the 8th generation

the senescent cell was identified by modified stained withβ-galactosidase（ SA-β-gal）

cell proliferation ability detection with CCK-8 and cell cycle analysis by flow cytometry. The cells were inoculated with 6 × 103 to 8 × 103 density per orifice in a 96-pore plate

and were divided into a young group

a senescent group

a resveratrol group and three Ext groups at low

middle

high dosage

3 multiple pores in each group. The young group was the 5th young generate cells

while others were the 8th generation of replicate senescent cells. The cells in resveratrol group were added with100 μl 10 μmol / L resveratrol solution

and the Ext groups at low

middle

high dosage were given 10 μl Ext with concentration of 50

100

or 200 mg / L

respectively. The morphology changes of filamentous actin（ F-actin） and globular actin（ G-actin） were observed after 24 h

48 h and 72 h of treatment. Results The positive staining index of SA-β-gal was significantly higher in the senescent group than that in the young group（ P < 0. 01）. The cells ratio of G0 / G1 cycle was increased

while the ratio of G2 / M was decreased

and the cell proliferation ability was obviously lower in the senescent group than in the young group（ P < 0. 01）. In the senescent group

the F-actin appeared broken

stress fibers and the G-actin was shown extending shift to cell surrounding area

and the cell central area was weak dyeing. While in the resveratrol group and Ext groups at low

middle

and high dosage

the microfilament structure of replicate senescent HCMEC was maintained

less G-actin to F-actin transformation and less stress fibers formed. The intervention effect grew with the intervention time. Conclusion The Ext maintaining the normal microfilament form of replicate senescent HCMEC might be the underlying important mechanism.