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Hepatic ischemia-reperfusion (ischemia-reperfusion, IR) injury is more common in liver transplantation , shock , liver surgery , clamping the portal vein or hepatic artery , etc. . Liver IR injury mechanism is not yet clear , may be related to apoptosis , reactive oxygen species , mitochondrial damage and endoplasmic reticulum stress . Previous studies have shown that the inhibition of apoptosis , can significantly reduce IR injury . Heme oxygenase (heme oxygenase, HO) is the starting enzyme of heme degradation and the rate-limiting enzyme in the body break down heme to generate carbon monoxide ( carbon monoxide , CO) , biliverdin and free iron . HO able to play a variety of biological effects of inhibition of apoptosis , and signal transduction . Studies show a protective role in rat liver IR injury , HO , improve liver function , reduce hepatocyte apoptosis . Objective: This study was designed by the application of inducers of HO - high chlorine heme (hemin) and application of the inhibitor of HO - observed HO-CO system , zinc protoporphyrin (ZnPP) on apoptosis of liver IR and related genes , research HO liver IR injury protection mechanisms . Methods: Preparation of an animal model : In this study, Sprague-Dawley (SD) rats after intraperitoneal injection of 10 % chloral hydrate (0.3ml/kg) anesthesia , take the abdominal incision Rufu revealed liver using micro the vascular clamp onto the hepatic artery and portal vein of the liver lobe and the left lobe , causing 70% of liver ischemia model . The jaws After 45 minutes , restore hepatic blood flow , liver IR model was prepared .
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