Eet alleviate the ischemia reperfusion injury of dcd in a rat liver transplantation model by regulating autophagy

Hepatic ischemia-reperfusion injury (IRI) is a common pathological phenomenon in clinical symptoms such as liver transplantation, liver tumor resection, major bleeding, and shock. Disorders of lipid metabolism in the ischemic stage are important lesions during liver ischemia-reperfusion injury. In this process, the up-regulation of 12-lipoxygenase (ALOX12) and the accumulation of 12-hydroxy eicosatetraenoate hydrazone (12-HETE) lead to metabolic regulation that precedes inflammation and cell death. Among them, 12-HETE can cause vascular endothelial cell dysfunction, inflammatory response and increased apoptosis to aggravate organ damage. EET is a subsequent oxidative metabolite of 12-HTHE. At present, in the study of cardiovascular and cerebrovascular, it is found that its biological effect is opposite to that of 12-HTHE, and it is involved in regulating cell autophagy to protect cell damage. Cell autophagy plays a protective role in alleviating cell damage, clearing oxidative stress damage, and inhibiting apoptosis during hypoxia injury. In this study, an animal model of hepatic ischemia-reperfusion was prepared using a surgical method, and EET, normal saline, and the untreated group were used as drug interventions. Observe the differences of apoptotic bodies and autophagosomes in different drug groups by electron microscopy. TUNEL sections were used to analyze the protective effects of different drug groups on animal models of ischemia-reperfusion. Cobalt chloride was used for hypoxia modeling, using EET, normal saline, and the untreated group as drug intervention. Use flow cytometry to analyze the effects of different drugs on model cells ‘ROS, calcium flow, and apoptosis; use ELISA to analyze the effects of different drugs on model cells’ inflammation; autophagy double-labeled virus and western blot combined to analyze the effects of different drugs on model building Autophagy effects in cells; 3-ma, an autophagy pathway blocker, further validates the role of different drugs through the autophagy pathway. Animal experiment results show that EET can significantly increase the autophagy level in the experimental group and reduce liver damage caused by IRI; cell experiment results show that EET mainly reduces the fear of ROS caused by hypoxia by increasing the autophagy level of cells Ascent, calcium flow increases and apoptosis increases.