Mitochondrial Homeostasis and Mast Cells in Experimental Hepatic Ischemia-Reperfusion Injury of Rats

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dc.authorid0000-0002-2778-8059tr
dc.contributor.authorKoç, Süleyman
dc.contributor.authorDoğan, Halef Okan
dc.contributor.authorKarataş, Özhan
dc.contributor.authorErdoğan, Mehmet Mustafa
dc.contributor.authorPolat, Vural
dc.date.accessioned2023-06-22T11:52:22Z
dc.date.available2023-06-22T11:52:22Z
dc.date.issued2022-10-22tr
dc.departmentSağlık Bilimleri Enstitüsütr
dc.description.abstractBackground: Ischemia-reperfusion injury is a histopathological event and is an important cause of morbidity and mortality after hepatobiliary surgery. We aimed to investigate the protective effect of uridine on hepatic ischemia-reperfusion injury in rats. Methods: The animals were divided into 4 groups (n = 8): group I (control), group II: ischemia-reperfusion (30 minutes ischemia and 120 minutes reperfusion), group III: ischemia-reperfusion+uridine (at the beginning of reperfusion), and group IV: ischemia-reperfusion+uridine (5 minutes before ischemia-reperfusion). Uridine was administered a single dose of 30 mg/kg IV. The 3 elements of the hepatoduodenal ligament (hepatic artery, portal vein, and biliary tract) were obliterated for 30 minutes. Then hepatic reperfusion was achieved for 120 minutes. Results: In the ischemia-reperfusion group, both liver tissues and serum chymase activity and high-temperature requirement A2 levels were higher. Severe central vein dilatation and congestion, widening sinusoidal range, diffuse necrotic hepatocytes and dense erythrocyte accumulation in sinusoids, and strongly inducible nitric oxide synthase expression were seen in the ischemia-reperfusion group. A clear improvement was seen in both uridine co-administration and pretreatment groups. Conclusion: Our results revealed that uridine limits the development of liver damage under conditions of ischemia-reperfusion, thus contributing to an increase in hepatocyte viabilitytr
dc.identifier.doi10.5152/tjg.2022.21911en_US
dc.identifier.endpage784tr
dc.identifier.issue7tr
dc.identifier.pmid35946882en_US
dc.identifier.scopus2-s2.0-85138457721en_US
dc.identifier.scopusqualityN/A
dc.identifier.startpage777tr
dc.identifier.trdizinid1134937en_US
dc.identifier.urihttps://www.turkjgastroenterol.org/en/mitochondrial-homeostasis-and-mast-cells-in-experimental-hepatic-ischemia-reperfusion-injury-of-rats-136935
dc.identifier.urihttps://hdl.handle.net/20.500.12418/13957
dc.identifier.volume33tr
dc.identifier.wosWOS:000865999100007en_US
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakTR-Dizinen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTURKISH JOURNAL OF GASTROENTEROLOGYtr
dc.relation.ispartofTURKISH JOURNAL OF GASTROENTEROLOGYen_US
dc.relation.publicationcategoryRaportr
dc.rightsinfo:eu-repo/semantics/openAccesstr
dc.subjectChymase, ischemia-reperfusion, liver injury, mast cells, uridinetr
dc.titleMitochondrial Homeostasis and Mast Cells in Experimental Hepatic Ischemia-Reperfusion Injury of Ratsen_US
dc.typeArticleen_US

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