The role of N-acetylcysteine in preventing hepatic injury associated with systemic oxidative stress after extracorporeal shock wave treatment

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dc.authoriderdem, havva/0000-0002-3074-0240
dc.authorwosiderdem, havva/E-9297-2015
dc.authorwosidCam, Sebahat/ABI-6218-2020
dc.contributor.authorCam, Sebahat
dc.contributor.authorBaba, Dursun
dc.contributor.authorSenoglu, Yusuf
dc.contributor.authorYuksel, Alpaslan
dc.contributor.authorErdem, Havva
dc.date.accessioned2021-12-01T18:49:46Z
dc.date.available2021-12-01T18:49:46Z
dc.date.issued2020
dc.department[Belirlenecek]en_US
dc.description.abstractBackground. Systemic oxidative stress may cause detrimental consequences for the liver, leading to hepatic fibrogenesis. Objectives. To investigate histopathological changes in liver tissues due to the increased systemic oxidative stress associated with rat extracorporeal shock wave lithotripsy (SWL) model and to document the consequences of N-acetylcysteine (NAC) administration. Material and methods. In this experimental SWL model, 18 Wistar albino rats were randomly assigned into 3 groups. The control group (group I) had no intervention. Group II underwent SWL treatment with intraperitonea I saline injection. Group III also had SWL with intra peritoneal NAC and was divided into short-term (group III-14 days) and long-term (group III-28 days) subgroup. Hepatectomy was performed for histopathological examinations. Histopathological alterations were evaluated with light microscopy. Immunohistological staining for p53 and myeloperoxidase was also performed. Results. Blood samples revealed a significant increase in plasma oxidative stress index (OSI) after plasma total antioxidant status (TAS) and total oxidant status (TOS) had been measured. It was shown that this increased systemic oxidative stress adversely affected liver tissues. Predominantly, sinusoidal dilatation was remarkably observed in rats with significantly high 051 values (p = 0.043). Similarly, periportal necrosis significantly increased in rats with high OSI values (p = 0.033). p53 positivity was also remarkable in rats with systemic oxidative stress (p = 0.049). N-acetylcysteine administration provided a significant decrease in OSI. N-acetylcysteine also improved all these alterations, including p53 staining. Particularly, sinusoidal dilatation was significantly protected in the long-term NAC group (group III-28 days). Conclusions. We demonstrated that SWL-induced systemic oxidative stress causes histological alterations in liver tissues. Increased p53 and myeloperoxidase staining as markers of oxidative damage were also detected. N-acetylcysteine may protect from these histological and ultra-structural alterations related to oxidative stress.en_US
dc.identifier.doi10.17219/acem/126294
dc.identifier.endpage1180en_US
dc.identifier.issn1899-5276
dc.identifier.issn2451-2680
dc.identifier.issue10en_US
dc.identifier.pmid33030315en_US
dc.identifier.scopus2-s2.0-85094819330en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1175en_US
dc.identifier.urihttps://doi.org/10.17219/acem/126294
dc.identifier.urihttps://hdl.handle.net/20.500.12684/10774
dc.identifier.volume29en_US
dc.identifier.wosWOS:000585073300006en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherWroclaw Medical Univen_US
dc.relation.ispartofAdvances In Clinical And Experimental Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectliveren_US
dc.subjectoxidative stressen_US
dc.subjectN-acetylcysteineen_US
dc.subjectsinusoidal dilatationen_US
dc.subjectp53en_US
dc.subjectAntioxidant Agenten_US
dc.subjectInflammationen_US
dc.subjectLithotripsyen_US
dc.subjectDiseasesen_US
dc.subjectFibrosisen_US
dc.subjectDamageen_US
dc.titleThe role of N-acetylcysteine in preventing hepatic injury associated with systemic oxidative stress after extracorporeal shock wave treatmenten_US
dc.typeArticleen_US

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