Journal List > Hanyang Med Rev > v.33(3) > 1044150

Kang: Experiment of Ischemia/Reperfusion Injury of the Cirrhotic Liver in the Murine Mouse Model

Abstract

As a medical doctor, the final goal of any type of research is focused on better treatment or contemporary care of the patient. As a surgeon, the research is focused on improving results in surgical procedure and improving the immediate to long term outcomes. In human beings, hepatobiliary tract and pancreas (HBP) play a major role in digestion, body metabolism and endocrine function. These organs are sophisticated in pathology as well as anatomy and physiology. The surgery of the hepatobiliary and pancreatic organ is very difficult. Therefore, the hepatobiliary surgeon's endeavor to treat patients who have hepatobiliary and pancreatic diseases should be scientific and based on evidence in order to get the best result.
Here I describe the topic of ischemia/reperfusion injury of the liver from my experience to establish safe surgical resection of the liver with limited bleeding and ischemia/reperfusion injury. Furthermore, I have added ischemia/reperfusion injury in the cirrhotic mouse model, methodology and brief result that I have achieved.

Figures and Tables

Fig. 1
Protocol of hepatic ischemia/reperfusion of the experimental mouse. (A) Intermittent clamping, five cycles of repeated ischemia for 15 minutes and reperfusion for 5 minutes. (B) Ischemic preconditioning, ischemia for 10 minutes and reperfusion for 15 minutes, then prolonged ischemia for 75 minutes. (C) Control, continuous 75 minutes ischemia.
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Fig. 2
Clamping of the portal triad of the mouse liver.
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Fig. 3
Intracellular signal pathway of apoptosis.
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Fig. 4
TUNEL stain. (A) Negative for TUNEL stains, (B) Positive for TUNEL stain, multiple green colored fluorescent stained nuclei are shown, which reflects injured DNA of the hepatocyte nucleus. Ref. 4 with permission from John Wiley and Sons.
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Fig. 5
DNA laddering. Agarose gel electrophoresis of DNA from livers after reperfusion for 3 hours. (A) Known markers are shown comparing the experimental material. (B) Varying ischemic insults showed no DNA laddering in both intermittent clamping. (C) By contrast, the livers subjected to continuous ischemia showed the typical laddering pattern indicating DNA fragmentation. Ref. 7 with permission from Elsevier.
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Fig. 6
Trichrome stained experimental mouse liver. (A) After intraperitoneal injection of 50% solution of CCl4 for 10 weeks. (B) After oral ingestion of thioacetamide solution for 10 weeks.
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Fig. 7
Isolated perfused rat liver model.
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Table 1
Protocol to induce hepatic cirrhosis of the mouse model
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PO per oral, IP intraperitoneal, *d/w distilled water; Per oral intake of CCl4 50% solution for 12 weeks is the most effective protocol to induce cirrhosis without less mortality.

References

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