| Objective: To investigate the effect of ghrelin at different concentrations on reactive oxygen species(ROS),endothelin-1(ET-1) and nitric oxide(NO) produced by human umbilical vein endothelial cells (HUVECs) under the induction of angiotensinⅡ(AngⅡ) in vitro, furthermore observe the protective effect of ghrelin on the injury of HUVECs induced by AngⅡ.Method: HUVECs cultured in vitro were randomly divided into 4 groups:Control group; Ghrelin group(10-7mol/L); AngⅡgroup(10-7mol/L); AngⅡ(10-7mol/L)+ Ghrelin groups (cells of groups were firstly incubated with 10-8mol/L,10-7mol/L,10-6mol/L human ghrelin respectively for 1h, then incubated with 10-7mol/L AngⅡ) . The cases of each group were 6. After being coincubated for 18 hours by AngⅡand ghrelin. Intracellular ROS levels were detected by flow cytometry(FCM), ET-1 and NO were measured by radioimmunoassay and nitrate reduction test respectively.Result: Exposure of HUVECs to AngⅡ(10-7mol/L) for 18h significantly increased HUVECs ROS production and ET-1 release (21.44±2.19 vs 2.95±0.89;111.33±7.90 vs 43.20±9.66;P<0.01,respectively),while NO production significantly decreased(26.63±3.62 vs 57.61±2.38,P<0.01); compared to the control group.Ghrelin caused a significant decrease the production of ROS and the release of ET-1,while significantly increased HUVECs the production of NO (P<0.05) induced by AngⅡ;and these effects were dose-dependent.but ghrelin(10-7mol/L) had nothing to do with the basal secretion of ROS and ET-1,as well as the release of NO(P>0.05).Conclusion: AngⅡ(10-7mol/L) can obviously stimulate the production of ROS and ET-1 and decrease NO secretion in HUVECs , Ghrelin(10-8mol/L～10-6mol/L) can protect HUVECs against injury induced by AngⅡas a result of the increased production of NO and inhibition of ROS and ET-1 secretion, and these effects are dose-dependent. but ghrelin(10-7mol/L) has nothing to do with the basal secretion of ROS and ET-1,as well as the release of NO.
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