| Summary: | 碩士 === 國立臺灣大學 === 解剖學暨生物細胞學研究所 === 98 === Introduction: Ischemic postconditioning (iPoC), a repetitive, brief ischemia- reperfusion maneuver performed at or before the initiation of tissue reperfusion, has been shown to mitigate reperfusion injury in heart and brain. The aim of this study is to investigate the effects of iPoC on liver ischemia- reperfusion injury.
Methods: Partial liver ischemia-reperfusion injury is induced by clamping the left lobes of liver for 45 minutes on male Wistar rats (160 g- 180 g). Three cycles of one-minute’s ischemia-reperfusion of the liver, performed by clamping and de-clamping of the liver, are applied before the commencement of reperfusion as the iPoC maneuver. Blood and liver samples are harvested at 240 minutes after reperfusion for end-point assessments which include serum GPT, H&E staining, TUNEL staining, and electron microscopy (EM) study. The results are compared between the sham, sham+ATR(atractyloside), control , postconditioning (iPoC) and postconditioning+ATR (iPoC+ATR) groups.
Results: Our data shows that there are no differences in the basal GPT levels of the five groups, but ischemic postconditioning could reduce the elevation of serum GPT level after reperfusion for 240 minutes (174.0±28.3 U/L v.s 416.3±16.7 U/L, p <0.05), and decrease the percentage of apoptotic hepatocytes(44.9±9.9 % v.s 81.1±13.8 %，p<0.05). The co-treatment with iPoC and ATR (iPoC+ATR) could increase the elevation of serum GPT and the number of apoptotic hepatocytes. There are no differences between iPoC+ATR and control groups in serum GPT level after reperfusion for 240 minutes (557.0±86.7 U/L v.s 416.3±16.7 U/L, p=0.18) and the percentage of apoptotic hepatocytes ((63.2±4.0 % v.s 81.1±13.8 %，p=0.09). EM study showed the morphology of mitochondria is more intact after reperfusion when compared to those in control group. Western blot shows increased cytochrome c expression in cytosol portion after reperfusion injury of liver, and postconditioning decreased the expression of cytochrome c after reperfusion. The co-treatment with iPoC and ATR could increase the expression of cytochrome c after reperfusion.
Conclusions: This study shows that ischemic postconditioning can attenuate cell deaths after reperfusion injury of liver. The mechanism of protection conferred by postconditioning is related to reduced cytochrome c release, and mediation of mitochondrial permeability transition pore (mPTP).
|
|---|
