Mechanism Of The Effect Of Apiin On HUVEC Hypertension Damage Model

In this paper, the apiin in celery was used as the research object, aiming at the key problems involved its pathway and repair mechanism in blood pressure regulation, the protection of apiin on HUVEC damage in hypertension model was studied, Besides, through the research of apiin’s effects the regulation of blood pressure by PI3K/Akt and NADPH-ROS signaling pathway by RT-PCR and Wesstern blot, we wanted to measure how dose apiin play the role in these pathways in vascular endothelial cell and what’s the mechanism. If we solve those problems above, we would provid the theory basis for research on celery as auxiliary hypotensive food. The results obtained are as follows:(1) Human umbilical vein endothelial cells were used as a model of carrier which was induced by hypertension related factors, such as Ang I, Ang II and H2O2 to establish HUVEC hypertension damage model. Through the investigation of the HUVEC morphological changes, cell activity, cell damage and cell function to evaluate the degree of model. Results showed that, except Ang I normal dose group (0.1 μM), the other inducers at each time point could induce HUVEC damage by oxidative stress, decreasing cell viability and the release of NO. Overall, the group of 0.1 μM Ang II induced 12 h could not cause cell death, had stronger ability to reduce the activity of cells about 22.9%, increase MDA to 4.89 nmol/mgprot(increased 1.7 times), decrease SOD activity to 31.62 mgprot/mL(decreased about 3 times). What’s more, the function factor of vascular endothelial cell NO release decreased to 32.33 μmol/L (decreased by 1.5 times), the activity of eNOS decreased to 0.26 U/mL(59 times lower), ET-1 did not change significantly. Comprehensive the above reason, it was chosen as the model of inducer to build damage model.(2)Apiin(40 μM) acted on HUVEC hypertension damage model could promote cell proliferation to increase the number of cells(up tol7.46%); reduce the release of MDA(6.34 to 1.93 nmol/mgprot), increase the activity of SOD(31.62 to 79.21 mgprot/mL) to reduce the occurrence of oxidative stress; at the same time, could increase the release of NO(28.82 to 48.26 μmol/L), enhance the activity of eNOS(1.81 to 13.63 U/mL), reduce the ET-1 production(10.15 to 5.68 ng/L) to improve the HUVEC function of regulating blood pressure, the function tends to be the same lever before being induced. The functional effect of apiin in low concentration (less than 50 μM) showed dose-dependent increase with time, but along with the increase of the dose (more than 50 μM), the efficacy of repairing cells decreased. Comprehensively comparing the effects of different doses apiin in different time, the final choice of apiin was 40 μM induced 12 h as the object for further research.(3)Apiin plays endothelial cell function repair of HUVEC damage in hypertension model is mainly through the activation of the PI3K/Akt signaling pathway, inhibition of the NADPH signaling pathway. Apiin could activate PI3K/Akt signal pathway to activate eNOS 1177 serine phosphorylation to promote NO release, this process could be inhibited by the NADPH signaling pathway, indicating apiin can inhibit NADPH peroxidase to increase NO release. What’s more, apiin function In ths model did not have an interactive relationship between PI3K/Akt signal pathway and NADPH signal pathway, which indicats that this process in vascular endothelial cells does not occur or be offset effect.