The Protection Of Human Umbilical Vein Endothelial Cells In Tert-Butyl Hydroperoxide-Induced Cell Injury Through Nrf2 Pathway By Z-Ligustilide

Background and ObjectiveAtherosclerosis(AS)is an important pathological basis of coronary atherosclerotic heart disease(CAS).Many studies have found that oxidative stress is an important patthological basis of AS.Nuclear factor E2 related factor(Nrf2)is a key factor in the human body trough its antioxidant,antioxidant and original(ARE)binding to start antioxidant genes downstream(heme oxygenase(HO-1),quinone oxidoreductase(NQO1),superoxide dismutase(SOD1),1 superoxide dismutase 2(SOD2),catalase(CAT)etc.)against oxidative stress,so to find effective activators of Nrf2 naturally become one of the new channel for AS.Z-Ligustilide is the active ingredients of Rhizoma Chuanxiong and has a wide range of pharmacological effect,such as anti-inflammatory,antioxidant,cardiovasc?lar protection.Our previous studies have demonstrated that Ningxintong gran?les have anti atherosclerotic plaque,but this mechanism on the cell?lar and molec?lar is unclear,so this study on human umbilical vein endothelial cells(HUVECs)as the research object,to explore the effect of Ningxintong gran?les in the main component of Z-Ligustilide."The key mechanism of intervention effect on endothelial cell injury of oxidative stress",explore the Yiqihuoxuefang Ningxintong mechanism of particle formation of AS,is further preparatory work and continuation.At the same time,it can provide a reference for further study on the inhibition of AS and the clinical treatment of AS by inhibiting the oxidative stress damage of vasc?lar endothelial cells.MethodHUVECs was c?ltured in vitro,and the cell viability of HUVECs were measured by MTT assay.The activation effect of Z-Ligustilide with different doses and different incubation time on ARE was detected by luciferase reporter assay.RT-PCR and Western Blot were used to determine the doses and time effects of Z-Ligustilide on the expression of the Nrf2 and its downstream gene HO-1,NQOl,SOD1,SOD2 and CAT in HUVECs.DCFH-DA fluorescence was used to observe intracell?lar ROS content in HUVECs.ResultsHere,our study demonstrated that Z-Ligustilide might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.The res?lts of our study indicated that Z-Ligustilide decreased the levels of intercell?lar reactive oxygen species(ROS)and increased the cell viability of HUVECs res?lting in protective effects against oxidativestress-induced cell damage in HUVECs.It suppressed oxidative stress damage by inducing the expression of Nrf2-reg?lated antioxidant enzyme genes such as HO-1,NQO1,SOD1,SOD2 and CAT in HUVECs.ConclusionThis study is the first to demonstrate that Z-Ligustilide suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.