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

dc.authorid0000-0002-3074-0240
dc.authorid0000-0002-3072-9252
dc.authorid0000-0002-4779-6777
dc.contributor.authorCam, Sebahat
dc.contributor.authorBaba, Dursun
dc.contributor.authorSenoglu, Yusuf
dc.contributor.authorYuksel, Alpaslan
dc.contributor.authorErdem, Havva
dc.date.accessioned2025-05-10T19:35:19Z
dc.date.issued2020
dc.departmentİstanbul Medeniyet Üniversitesi
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.
dc.identifier.doi10.17219/acem/126294
dc.identifier.endpage1180
dc.identifier.issn1899-5276
dc.identifier.issn2451-2680
dc.identifier.issue10
dc.identifier.pmid33030315
dc.identifier.scopus2-s2.0-85094819330
dc.identifier.scopusqualityQ1
dc.identifier.startpage1175
dc.identifier.urihttps://doi.org/10.17219/acem/126294
dc.identifier.urihttps://hdl.handle.net/20.500.14730/8820
dc.identifier.volume29
dc.identifier.wosWOS:000585073300006
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWroclaw Medical Univ
dc.relation.ispartofAdvances in Clinical and Experimental Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250302
dc.subjectliver
dc.subjectoxidative stress
dc.subjectN-acetylcysteine
dc.subjectsinusoidal dilatation
dc.subjectp53
dc.titleThe role of N-acetylcysteine in preventing hepatic injury associated with systemic oxidative stress after extracorporeal shock wave treatment
dc.typeArticle

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