Abstract：Objective To explore the effects of liraglutide, a GLP-1 analogue, on CMECs and the mechanisms by which liraglutide reduces the oxidative stress apoptosis of CMECs under a hypoxia/reoxygenation (H/R) model.Methods In vitro cultured CMECs of SD rats were purified with the differential adhesion method and identified immunocytochemically using CD31 antibody. GLP-1R and CD31 were assessed by co-location immunohistochemistry. MTT assay was performed to assess the proliferation of the first-generation cells exposed to different concentrations (0-100 nM) of liraglutide. An H/R model was used to induce cellular apoptosis, and the apoptotic rate was assessed by low cytometry. DCFHDA was used to evaluate the ROS contents. Western blot and immunohistochemistry were used to assess the expressions of XO and caspase3. The expressions of XO, ROS and caspase3 in each group were compared to illustrate the liraglutide-mediated anti-apoptotic functions.Results The H/R model induced a higher expression of XO, and consequently generated excessive ROS which was responsible for cellular apoptosis (20.66%±1.30%). Lirglautide pretreatment for 12 h could suppress the XO activation, ROS outburst and cellular apoptosis (8.36%±1.19%).Conclusions This study has confirmed that H/R can induce CMECs’ oxidative damage through the XO-ROS injury signals, and that liraglutide pretreatment may suppress such damage to CMECs.
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2018, Vol. 29 
