Ulinastatin alleviated Lps-induced injury of cardiac micro vascular endothelial Cell via NF-κB pathway.

The aim of this study to investigate the effect of ulinastatin (UTI) on lipopolysaccharide (LPS) -induced injury of cardiac micro vascular endothelial cell, and explore potential mechanisms Primary cardiac micro vascular endothelial cells were harvested from neonatal Sprague Dawley rats. Cardiac micro vascular endothelial cells were prepared for further treatment after subculture. The experiment was designed into 4 groups: Control group, LPS (0.1U/ml) group, UTI (100U/ml) group and (UTI+LPS) group. MTT assay and scratch test were performed to assess cell viability of cardiac micro vascular endothelial cells. Flow cytometry was performed to examine apoptosis. Western blot was performed to examine expression of multiple proteins, including pAkt, Bcl-2, NF-κB, TNF-α and Caspase-3. Compared with control group, LPS treatment indeed increased protein expression of Caspase-3, and resulted in significant apoptosis of cardiac micro vascular endothelial cells. Compared with LPS group, UTI+LPS group had a higher level of cell viability, verified by MTT assay and scratch test. Moreover, expressions of pAkt, NF-κB and Bcl-2 were decreased after UTI treatment, suggesting UTI significantly alleviated LPS induced-apoptosis of cardiac micro vascular endothelial cell via Akt/NF-κB pathway. Ulinastatin could protect cardiovascular system by alleviating LPS-induced injury of cardiac micro vascular endothelial cell. The potential mechanism is Akt/NF-κB pathway.