Objective: To explore the effect of end stage renal disease (ESRD) serum on apoptosis in human umbilical vein endothelial cells and the intervention action by total flavonoids of astragalus in this process. Method: The serums of 22 healthy volunteers and 25 patients with ESRD undergoing regular hemodialysis were collected. Simulating ESRD environment in vitro

human umbilical vein endothelial cells (HUVECs) were selected as the subject. Then they were divided into blank control group (including 10% fetal calf serum)

normal control group (including 10% healthy serum)

ESRD group (including 10% ESRD serum)

low dose group

medial dose group and high dose group with total flavonoids of astragalus (0.5

1.0

2.0 g·L-1 total flavonoids of astragalus

respectively). After being culturing for 24 hours

the morphological change of endothelial cells were observed by microscopy

survival rate was detected by MTT test

the expression of C/EBP homologous protein (CHOP) was examined by immunohistochemical staining

the content of 4-hydroxynonenal (HNE) was detected by ELISA

and the morphological change of apoptosis was observed by TUNEL method. Result: Comparing with the normal control group

HUVECs survival rate was lower in ESRD group(P<0.01)

CHOP

4-HNE(P<0.05) and apoptosis index(P<0.01) were increased. The total flavonoids of astragalus could significantly increase the survival rate of HUVECs(P<0.05)

and decrease the expression of CHOP(P<0.05). Besides

better results were found in medial dose group than low dose group(P<0.01)

but no statistically significant difference were found between high dose group and middle does group. Morever

the total flavonoids of astragalus could decrease 4-HNE and the apoptosis index(P<0.05)

and the effect is dose-dependent(P<0.05). Positive correlation were found between CHOP and 4-HNE(P<0.01). Conclusion: ESRD serum could induce HUVECs apoptosis

and the mechanism may be related to endoplasmic reticulum stress. Total flavonoids of astragalus could inhibit endothelial cell apoptosis induced by ESRD serum through alleviating endoplasmic reticulum stress.