{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T21:14:13Z","timestamp":1793049253444,"version":"4.5.0"},"reference-count":45,"publisher":"Canadian Science Publishing","issue":"2","license":[{"start":{"date-parts":[[2017,4,1]],"date-time":"2017-04-01T00:00:00Z","timestamp":1491004800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Biochem. Cell Biol."],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:p> The study was carried out to define whether prednisolone-induced damage to hepatic cells is accompanied by excessive nitric oxide (NO) levels associated with nuclear factor kappa B (NF-\u03baB)\/inducible NO synthase (iNOS) activation and evaluate the efficacy of the treatment with vitamin D<jats:sub>3<\/jats:sub>. Histopathological examination, activities of liver transaminases (alanine aminotransferase and aspartate aminotransferase), and cell death assays consistently showed that prednisolone (5 mg\/kg body weight, 30 days) induces chronic liver injury in female Wistar rats. Specifically, increased hepatocellular necrosis and caspase-3-dependent apoptosis were observed. Prednisolone enhanced iNOS protein expression, NO generation, and tyrosine nitration in liver cells. Despite unchanged hepatic level of the NF-\u03baB\/p65 protein, prednisolone increased inhibitory \u03baB-\u03b1 (I\u03baB-\u03b1) degradation, nuclear translocation, and phosphorylation of NF-\u03baB\/p65 at Ser311, indicating that NF-\u03baB activation can be involved in the induction of iNOS\/NO. All changes were associated with a 2.9-fold decrease in the serum content of 25-hydroxyvitamin D<jats:sub>3<\/jats:sub> and significant reduction of hepatic vitamin D<jats:sub>3<\/jats:sub> receptor (VDR) expression that points reliably to vitamin D<jats:sub>3<\/jats:sub> deficiency and failures in VDR signaling. Vitamin D<jats:sub>3<\/jats:sub> co-administration (100 IU\/rat, 30 days) prevented glucocorticoid-evoked abnormalities in hepatic tissue. In conclusion, prednisolone-induced liver disturbances were associated with the impairment of NF-\u03baB\/iNOS\/NO responses that can be ameliorated by vitamin D<jats:sub>3<\/jats:sub> treatment through VDR-mediated mechanisms. <\/jats:p>","DOI":"10.1139\/bcb-2016-0070","type":"journal-article","created":{"date-parts":[[2016,7,14]],"date-time":"2016-07-14T22:02:43Z","timestamp":1468533763000},"page":"213-222","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":25,"title":["Vitamin D<sub>3<\/sub> protects against prednisolone-induced liver injury associated with the impairment of the hepatic NF-\u03baB\/iNOS\/NO pathway"],"prefix":"10.1139","volume":"95","author":[{"given":"Olha","family":"Lisakovska","sequence":"first","affiliation":[{"name":"O.V. Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, 01601, Leontovich str., 9, Kyiv, Ukraine."},{"name":"O.V. 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