Fig. 4

Sufentanil attenuates Cx43 channel function on HUVECs, with no effect on ATP and ADO release. a Sufentanil inhibits dye coupling between HUVECs, but fentanyl and remifentanil do not have this effect (n = 4, *P < 0.05 vs control). The dye spread between HUVECs is detected by dye-coupling assay. The number of receiver cells around donor cell are normalized to control. b Fentanyl, sufentanil, and remifentanil induced no cytotoxicity in HUVECs (n = 5). Cell vitality is detected using cell counting kit-8 kit assays. The data of absorbance are normalized to control. c Fentanyl, sufentanil and remifentanil have no effects on Cx43 expression in HUVECs (n = 5). Cx43 expression is detected by western blotting. The gray values of blots are normalized to control. d Fentanyl, sufentanil, and remifentanil have no effects on ATP release from HUVECs (n = 6). ATP release is detected with ATP bioluminescence assay kits. The intensity of bioluminescence is normalized to control. e Fentanyl, sufentanil, and remifentanil have no effects on the ADO content from HUVECs (n = 6). The ADO content is detected using related ELISA kits. The data of absorbance are normalized to control. Fentanyl (Fen): 10 μg/ml, for 24 h; sufentanil (Suf): 25 ng/ml, for 24 h; remifentanil (Remi): 50 ng/ml, for 24 h. ADO, adenosine; HUVEC, human umbilical vein endothelial cell. All experiments are conducted in the presence of TNF-α. All data are presented as mean ± S.D.. Multiple comparisons among groups are performed using repeated-measures one-way analyses of variance, followed by Tukey post hoc comparisons