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Lemon extract reduces the hepatic oxidative stress and persulfidation levels by upregulating the Nrf2 and Trx1 expression in old rats
dc.creator | Miler, Marko | |
dc.creator | Živanović, Jasmina | |
dc.creator | Ajdžanović, Vladimir | |
dc.creator | Milenkovic, Dragan | |
dc.creator | Cesar, Thais | |
dc.creator | Filipović R., Miloš | |
dc.creator | Milošević, Verica | |
dc.date.accessioned | 2024-01-11T12:38:16Z | |
dc.date.available | 2025-01-09 | |
dc.date.issued | 2024 | |
dc.identifier.issn | 0951-6433 | |
dc.identifier.uri | https://iubmb.onlinelibrary.wiley.com/journal/18728081 | |
dc.identifier.uri | http://radar.ibiss.bg.ac.rs/handle/123456789/6462 | |
dc.description.abstract | Citrus flavanones are recognized as promising bioactives within the concept of healthy aging. Thus, the present study investigated the effects of a nutritionally relevant dose of lemon extract (LE) on liver redox regulation and persulfidation levels in 24-month-old Wistar rats. LE (40 mg/kg b.m.) was administered orally once daily for four weeks. Control groups received either vehicle (sunflower oil) or remained intact. The applied methodology considered qPCR, Western blot, protein persulfidation levels evaluation, histochemistry in line with immunofluorescence, liver biochemical assays (glutathione, total -SH groups and malonaldehyde; MDA), liver enzymes in serum and in silico analysis to explore the potential interaction/binding between the proteins studied in the paper. Our results showed that LE increased glutathione peroxidase (GPx), reductase (GR), glutamate-cysteine ligase catalytic and modifier subunit, respectively, as well as Nrf2 gene expressions, but decreased the expression of superoxide dismutase 2 (SOD2). Upon LE application, protein expression showed upregulation of NRF2, SOD2, GPx, GR, and thioredoxin 1 (Trx1). LE significantly decreased the protein persulfidation levels and concentration of MDA, a marker of oxidative damage in the cell. Histological analysis showed a normal liver histoarchitecture without pathological changes, aligning with the normal serum level of hepatic enzymes. Obtained results showed that LE, by modulating hepatic redox regulators Nrf2 and Trx1, diminishes oxidative stress and alters the persulfidation levels, suggesting a considerable beneficial antioxidant potential of lemon flavanones in the old-aged liver. | sr |
dc.language.iso | en | sr |
dc.publisher | John Wiley and Sons | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/inst-2020/200007/RS// | sr |
dc.rights | embargoedAccess | sr |
dc.source | Biofactors | sr |
dc.subject | citrus flavanone | sr |
dc.subject | eriocitrin | sr |
dc.subject | MDA | sr |
dc.subject | glutathione peroxidase/reductase | sr |
dc.subject | H2S producing enzymes | sr |
dc.subject | molecular docking analysis | sr |
dc.title | Lemon extract reduces the hepatic oxidative stress and persulfidation levels by upregulating the Nrf2 and Trx1 expression in old rats | sr |
dc.type | article | sr |
dc.rights.license | ARR | sr |
dc.rights.holder | © 2023 International Union of Biochemistry and Molecular Biology | sr |
dc.description.note | This is the peer reviewed version of the following article: Miler M, Živanović J, Ajdžanović V, Milenkovic D, Cesar T, Filipović MR, Milošević V. Lemon extract reduces the hepatic oxidative stress and persulfidation levels by upregulating the Nrf2 and Trx1 expression in old rats. BioFactors. 2024;, which has been published in final form at [https://doi.org/10.1002/biof.2038]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited. | |
dc.identifier.doi | 10.1002/biof.2038 | |
dc.type.version | acceptedVersion | sr |
dc.citation.rank | M21~ |