Protective effects of α-tocopherol and ischemic preconditioning on hepatic reperfusion injury
Tóm tắt
This study evaluated the effect of α-tocopherol (α-TC), íschemic preconditioning (IPC) or combination on the extent of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R). Rats were pretreated with α-TC (20 mg/kg per day, i.p.) for 3 days before sustained ischemia. A rat liver was preconditioned with 10 min of ischemia and 10 min of reperfusion, and was then subjected to 90 min of ischemia followed by 5 h or 24 h of reperfusion. I/R increased the ami-notransferase activity and mitochondrial lipid peroxidation, whereas it decreased the mitochondrial glutamate dehydrogenase activity. αand IPC individually attenuated these changes. αcombined with IPC (α-TC+IPC) did not further attenuate the changes. The mitochondrial glutathione content decreased after 5 h reperfusion. This decrease was attenuated by α-TC, IPC, and α-TC+IPC. The significant production of peroxides observed after 10 min reperfusion subsequent to sustained ischemia was attenuated by αIPC, and α-TC+IPC. The mitochondria isolated after I/R were rapidly swollen. However, this swelling rate was reduced by α-TC, IPC, and α-TC+IPC. These results suggest that either αor IPC reduces the level of mitochondrial damage associated with oxidative stress caused by hepatic I/R, but αcombined with IPC offers no significant additional protection.
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