Objective To explore the protective effect of
propofol on
endothelial cells during
heat stress and its protective effect to mitochondra.
Methods Heat stress model of
human umbilical vein endothelial cell was established when
cells were incubated at 43℃ for 2h, then further incubted at 37℃, 5%CO2 for 6h. The experimental group was subdivided into six groups, including 37℃ group, 37℃ plus intralipid group (negative
control group), 37℃ plus
propofol group, 43℃ plus
propofol group, 43℃ plus intralipid group, H2O2 plus
propofol group (positive
control group); Pretreated with 50μmol/L
propofol, 0.2ml intralipid or 25μmol/L H2O2 before
heat stress at 43℃, while the
cells in the
control group were incubated at 37℃.
Cell viability was tested by
CCK-8. ROS,
mitochondrial membrane potential and the changes in
mitochondrial permeability transition pore were determined by
flow cytometry. The level of
ATP was detected by
fluorescein-
luciferase. The changes of
caspase-9 and
caspase-3 were analyzed by
Caspase Activity Assay Kit. Results HUVESs
cell viability and damage of mitochondra were significantly decreased after
heat stress. Compared with 43℃
heat stress group, pretreatment with
propofol induced the recovery of
cell viability and the ROS levels were significantly decreased in
HUVEC cells (P<0.05). Meanwhile, the number of
cells representing the decrease of
mitochondrial membrane potential (the proportion of JC-1 monomer) was significantly decreased (P<0.05) by
propofol. The average
fluorescence intensity of calcein which representing the
MPTP changes and intracellular
ATP content was significantly increased (P<0.05). In addition, the activation of mitochondrial apoptotic pathway mediated by
caspase-9/3 was also inhibited. Conclusions
Propofol have anti-oxidative, anti-
apoptosis and
mitochondria protective effect against
endothelial cell injury during
heat stress.