Figure 1 | Cell Death Discovery

Figure 1

From: Unacylated ghrelin prevents mitochondrial dysfunction in a model of ischemia/reperfusion liver injury

Figure 1

Evaluation of liver mitochondrial membrane potentials (Δψ) and lag phase time. (a) Hepatic I/R injury experimental design: 10 Wistar rats underwent vascular clamp occlusion of the artery (ischemia), perfusing 70% of the liver. After 90 min of ischemia, the clamp was removed and reperfusion allowed for 2 h. Animals were then killed and mitochondria were isolated from the 70% of liver exposed to I/R and from the remaining 30%, which was used as an internal control. Either UnAG (100 μg/kg) or saline were injected into the hepatic artery 15 min before ischemia. (b) TPP+ electrode traces of liver mitochondria recovered from animals subjected to I/R or not, either treated or untreated with UnAG (100 μg/kg): at time 0 the mitochondrial preparation was energized with succinate, and Δψ quickly reached a physiological value. The time required for ETC to reestablish a pre-phosphorilative Δψ value after ADP administration corresponds to the Lag Phase time. Data are reported as mean±S.E.M. and representative of five different experiments, performed in triplicate (N=5). (c) Quantitative analysis of the Lag Phase time values, evaluated in liver mitochondria recovered from animals treated as indicated (*P<0.05 UnAG+I/R versus I/R). Data are reported as mean±S.E.M. and representative of five different experiments, performed in triplicate (N=5).

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