| Ischemic preconditioning (IPC) can protect the heart and blood vessel against the anoxia-reoxygenation injury (H/R), and the protection effect occur in not only the myocardial cell but also the endothelial cell. Medicament preconditioning can simulate or waken the body internal substance with drug to bring the protection effect. The study method is established to simulate the ischemic preconditioning ,too.First, our experimentation estsblish vessel endothelial cell H/R model. and study the injury effect about the anoxia and H/R. Then investigate the protection effect mechanism in captopril.To explore the mechanism of H/R and the late protective effect of catopril on endothelial cells(ECs). To establish anoxia-reoxygenation model on human unbilical veins endothelial cell line ECV304,and observe the injury degree of anoxia and reoxygenationg at the different time.Then these ECs were randomly divided into 5 groups: catopril, catopril+ bradykininβ2 receptor inhibitor,catopril+ PKC inhibitor, catopril+NOS inhibitor, catopril+NF-KB inhibitor,and observe the cell morphologic changes, mortality and the activities of malondialdehyde(MDA),superoxide dismutase(SOD),glutathione peroxidase(GSH-PX). Results show us after treatment with anoxia and anoxia-reoxygenation,the ECs' morphologic changes were observed.The mortality increased and MDA concentration became higher, the concentration of SOD and GSH-PX became lower(P<0.01). Meanwhile,the changes became more obviously with the time extending.The late preconditioning with catopril, the cell morphologic,MDA,SOD and GSH-PX keep normal.The protective effect became strenghen along with the catopril concentration increasing.However, culturing with above four inhibitors ,the protective effect was partly diminished. Thus we consider anoxia and anoxia-reperfusion induce lipid peroxidation and the weakening of antioxidation ability in a time-dependented manner. The late preconditioning with catopril can weaken anoxia-reperfusion injury in a concentration- dependented manner. Bradykinin β2 receptor, PKC activating ,nitric oxide and nucleus factor are all involved in the protective effect.To observe the expressions of ET-1,NO and NOS in the anoxia-reoxygenation injury(H/R) to human umbilical vein endothelial cells(EC),and further research the molecular mechanism of effect of catopril on production of ET-1 and NO. The third passage of cultured EC was randomly divided into 7 groups: normal(C), anoxia(H), anoxia-reoxygenation(H/R), catopril(CAP), catopril+ bradykinin Β2 receptor inhibitor,catopril+ PKC inhibitor, catopril+NF-ΚB inhibitor.Tatol RNA was extracted .The expression of ET-1,eNOS and iNOS mRNA were analyzed by semi-quantiative RT-PCR methed.The protein level of total NOS and NO were analysisde too. Results show us compared with C group, ET-1 mRNA expression increased significantly in H group and H/R group, and increased in three inhibitor groups. Compared with H/R group, ET-1 mRNA expression decreased in CAP group and three inhibitor groups, Compared with CAP group, ET-1 mRNA expression increased in three inhibitor groups. While the mRNA expressions of iNOS and eNOS were contrary to that of ET-1,and the change of iNOS was slightly. The protein levels of total NOS and NO are lower in H group and H/R group than in C group, higher in CAP group than in H group or H/R group,and those were lower in three inhibitor groups than in CAP group,however higher than in H/R group. Thus we consider The expression of ET-1 increased, while that of NO decreased in anoxia and anoxia-reoxygenation injury .Catopril can protect the imbalance of ET-1 and NO. Bradykinin Β2 receptor, PKC activating and nucleus factor are all involved in the protective effect. To explore the mechanism of apoptosis in anoxia-reoxygenation injury on endothelial cells and the late protective effect of catopril. To establish anoxia-reoxygenation model on human unbilical veins endothelial cell line ECV304, These ECs were randomly divided into 7 groups: different hypoxia...
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