Protective Effect of Over-expression OGCP on HEK293 Cells Treated by Rotenone and Mutant Parkin Protein

Objective To study the effect of α-ketoglutarate carrier protein(2-oxoglutarate carrier protein,OGCP) and the Parkin protein on HEK293 cell function.Methods The cell apoptosis rate,mitochondrial membrane potential and intracellular reactive oxygen species of HEK293 cells treated with rotenone,OGCP and / or Parkin protein were detected by using flow cytometry methods(FCM).Results ① Over-expression wild-type Parkin protein and /or OGCP can increase mitochondrial membrane potential of HEK293 cells induced by rotenone,reduce intracellular reactive oxygen species and cell apoptosis rate of HEK293 cells induced by rotenone,while over-expression mutant Parkin(R42P and T240R) protein can decrease the mitochondrial membrane potential of HEK293 cells,especially the HEK293 cells induced by rotenone,but increase intracellular reactive oxygen species and promote apoptosis.② In addition,we also found that OGCP can inhibit the increasing of mitochondrial membrane potential and reactive oxygen species and decreasing of cell apoptosis caused by mutant Parkin protein(R42P and T240R).Conclsuion ① Parkin protein and OGCP may be associated with the maintenance of normal function of mitochondria.② Over-expression of mutant parkin(R42P and T240R) protein may inhibit mitochondrial function and promote apoptosis.③ Over-expression OGCP has protective effect on cell toxicity caused by rotenone and mutant parkin protein.