Related Experiment Video
Updated: Jul 14, 2026
Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia
Published on: July 31, 2017
Protective effects of combined ischemic preconditioning and ascorbic acid on mitochondrial injury in hepatic
Woo-Yong Lee1, Jun-Seok Lee, Sun-Mee Lee
1College of Pharmacy, Sungkyunkwan University, Suwon, South Korea.
Background:
This study examined the in vivo effects of ischemic preconditioning (IPC), ascorbic acid (AA), or a combination (IPC + AA) on the level of mitochondrial injury caused by hepatic ischemia/reperfusion (I/R).
Materials And Methods:
A rat liver was preconditioned with 10 min of ischemia followed by 10 min of reperfusion, and then subjected to 90 min of ischemia followed by 5 h of reperfusion. The rats were pretreated with AA (100 mg/kg, i.v.) 5 min before the sustained ischemia.
Results:
I/R increased the aminotransferase activity and level of mitochondrial lipid peroxidation, whereas it decreased the reduced glutathione:oxidized glutathione ratio. Either the IPC or AA pretreatment alone attenuated these changes, with the effect being enhanced by IPC + AA. The level of mitochondrial glutamate dehydrogenase, which is specifically located in the matrix, decreased after I/R but this was prevented by IPC + AA. Significant peroxide production was observed after 10 min of reperfusion after sustained ischemia. This change was attenuated by either IPC or AA alone and was further attenuated by IPC + AA. The mitochondria isolated after I/R were rapidly swollen, indicating an opening of the permeability transition pore. However, this was markedly reduced by IPC + AA. The hepatic ATP level was lower after I/R, which was restored by IPC alone and IPC + AA.
Conclusions:
Our findings suggest that IPC and AA synergistically reduce the level of mitochondrial damage during I/R as a result of decreased postischemic oxidant stress.
