Propofol Attenuates Human Proximal Renal Tubular Epithelial Cell Injury Induced by Anoxia-Reoxygenation

We undertook a study to determine whether propofol pretreatment may protect human proximal renal tubular epithelial (HK-2) cells against anoxia-reoxygenation injury and the role of p38 mitogen-activited protein kinase (p38MAPK). HK-2 cells were randomly divided into 5 groups: a control group (Con); a group treated for 1 hour, cultured with with 300 μM CoCl2 normal medium for 24 hours, then stimulated with no serum media (group CoCl2); a group where the HK-2 cells were pretreated with 5μg/mL−1 propofol for 1 hour, then were treated as group (group Pro); a group where we pretreated CoCl2 the HK-2 cells with 10% intralipid 90 μL for 1 (group Int); hour, then treated as group CoCl2 and a group where we pretreated the HK-2 cells with propofol for 1 hour, 10 μmol/L−1SB203580 were (inhibitor of p38MAPK), and 300 μM CoCl2 added at the same time, then cultured with normal medium for 24 hours (group SB). Using MTT method and flow cytometry to detect the proliferation and apoptosis of HK-2 cells, the reverse transcriptase-polymerase chain reaction method was used to investigate the regulation of Bcl-2 and caspase-3 mRNA; the expression of p38MAPK was measured by Western blot. After pretreated with 5 μg/mL−1 propofol, HK-2 cell proliferation increased and apoptosis decreased (P<0.05 or 0.01). Intralipid did not effect HK-2 cells, the expression of Bcl-2 gene was upregulated, and caspase-3 gene was down-regulated. Meanwhile, the expression of p38MAPK was upregulated after propofol pretreament. These regulations can be reversed by SB203580 (P<0.05 or 0.01) with no difference between group Int and group CoCl2. Pretreatment with 5μg/mL−1 propofol protected HK-2 cells against anoxia-reoxygenation injury at clinically relevant concentrations by regulating the expression of apoptosis related genes. P38MAPK plays an important role in propofol protective effect.