Abstract:

Objective　To investigate the protective effect of carnosine on apoptosis in HBMEC induced by LPS and its mechanisms.　Methods　The injury model was established by treating HBMEC cells with LPS in vitro. Inverted microscope was used to observe cell morphology. The cell viability was detected by MTT assay, and the cell apoptosis rates were measured by flow cytometry. The reactive oxygen species (ROS) level in cells was detected by fluorescent probe CDFH-DA. The expressions of NF-κB P65, IL-1β and TNF-α were explored by Western blot.　Results　Compared with control group, the cell viability was slightly decreased in LPS group (P＞0.05). The apoptosis rate, the level of ROS, nuclear NF-κB P65, IL-1β and TNF-α increased obviously (P＜0.01) in LPS group. Compared with LPS group, the apoptosis rate, the level of ROS, nuclear NF-κB P65, IL-1β and TNF-α reduced obviously (P＜0.01) in LPS+carnosine group (10mmol/L,20mmol/L,40 mmol/L).　Conclusions　Carnosine has protective effect on apoptosis of HBMEC cells injury induced by LPS. The mechanism may be related that carnosine inhibited LPS induced ROS production, avoided NF-κB pathway overactivation, and further decreased the secretion of IL-1β and TNF-α.

Key words: Carnosine, 　LPS, 　HBMEC cells, 　Apoptosis, 　NF-&kappa, B