Effects Of Mitochondrial Miters On Energy Metabolism In Rat Model Of Oxygen Sugar Deprivation / Reoxygenation In Hippocampus Of Rats

Objective To investigate the effect of mitochondrial division inhibitor (mdivi-1) on energy metabolism and neuronal apoptosis induced by ischemia reperfusion injury (IRI).Methods We divided the primary cultured hippocampus cells into four groups: Control group(C), Vehicle group(V), mdivi-1plus ischemia reperfusion group(M), Ischemia reperfusion group (I). We established the model of ischemia reperfusion by the method of oxygen glucose deprivation, and before ischemia reperfusion group M was pretreated with mdivi-1for40min. After ischemia for6h and reperfusion for20h of hippocampus cells, we examined the expression of protein Drp1、Bc1-2/Bax by western blot and examined ATP content、mitochondrial complex activity、Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity with enzyme standard instrument.Results Our results showed that ATP content、mitochondrial complex activity、 Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity all decreased in Group M and I, compared with that in Group C(P<0.05); Group M markedly reduce the expression of protein Drp-1、Bax, and improve the expression of protein Bcl-2, increase the brain ATP content(74.129±5.773μmol/gprot), Na+-K+-ATPase(4.348±0.451U/mgprot) and Ca2+-Mg2+-ATPase activity(1.955±0.287U/mgprot), mitochondrial complex activity Ⅰ～Ⅳ(15.445±1.699nmol/(min-mg)、17.065±1.070nmol/(min-mg)、32.123±1.652nmol/(min-mg)、2.814±0.180nmol/(min·mg)), in varying degrees, compared with Group Ⅰ (P<0.01).Conclusion These findings indicated that mdivi-1,which inhibit mitochondrial fission, significantly improved mitochondrial energy metabolism and ameliorated cerebral ischemia/reperfusion injury.