Protective effect of cycloartenyl ferulate on lipopolysaccharide induced endothelial cell apoptosis and its mechanism / 中华急诊医学杂志

ABSTRACT

Objective@#To investigate the effect of cycloartenyl ferulate (CF) on lipopolysaccharide (LPS)-induced apoptosis in human umbilical vein endothelial cells (HUVEC), and to explore its relative mechanism.@*Methods@#Human umbilical vein endothelial cells were cultured in vitro, and the experiment was divided into the normal group, CF group, LPS group, and LPS+CF groups at different concentrations. After the corresponding treatment of cells in each group, the cell viability and apoptosis of each group were tested by the cell counter Kit-8 (CCK-8) assay and TdT-mediated dUTP nick end labeling (TUNEL) assay. The protein expression of Bax, Bcl-2, caspase-3 and the effect of CF on the protein expression of Nrf2/HO-1 pathway were determined by Western blot. One-way ANOVA were performed in multigroup mean comparison, LSD-t test was used to compare the mean values of two samples, and P<0.05 was considered statistically significant.@*Results@#Compared with the LPS group, the survival rate of HUVECs cells in the CF group was significantly increased with different doses, and the survival rate increased significantly in the 320 μmol/L CF group [(69.85±1.2)% vs ( 100.2±1.824)%, P< 0.01]. TUNEL staining showed that compared with the LPS group, the number of apoptotic positive cells in the 320 μmol/L CF group was significantly reduced [(27.33 ± 3.40) vs (11.67 ± 2.04), P<0.01]. Compared with the LPS group, Bcl-2 protein expression level was significantly increased in the CF group at different doses (P<0.01), caspase-3 and Bax protein expression were significantly decreased (P<0.01). Nrf2 protein expression level increased significantly (P<0.01), and HO-1 protein level increased significantly (P<0.01).@*Conclusion@#CF can alleviate LPS-induced apoptosis of HUVEC, which may be related to the increase of bcl-2 expression, the decrease of caspase-3 and Bax protein expression and the activation of Nrf2/ HO-1 signaling pathway.