{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T16:25:13Z","timestamp":1780590313825,"version":"3.54.1"},"reference-count":32,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2025,7,24]],"date-time":"2025-07-24T00:00:00Z","timestamp":1753315200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,7,24]],"date-time":"2025-07-24T00:00:00Z","timestamp":1753315200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Ochratoxin A (OTA) is a hepatotoxin that has considerable public health consequences. This study examined the protective benefits of isoliquiritigenin (ISL) against OTA\u2010induced hepatic toxicity in Swiss albino mice, with a focus on the Nrf2 signalling pathway. The mice were categorized into four groups: Group I (control): single daily dose of 0.05% DMSO was administered for 6 weeks. Group II (OTA): treatment with OTA at a dosage of 25\u2009mg\/kg body weight three times per week. Group III (OTA\u2009+\u2009ILS): treatment with OTA (25\u2009mg\/kg, three times per week) in combination with ILS at a single dose of 75\u2009mg\/kg daily (oral gavage). Group IV (ILS): treatment with ILS alone at a single dose of 75\u2009mg\/kg daily. The injection of OTA increased the levels of liver enzyme markers, indicating hepatic damage. Moreover, OTA elicited oxidative stress, as demonstrated by elevated lipid peroxidation and diminished antioxidant enzyme activity. OTA blocked the PI3K\/AKT\/Nrf2 signalling pathway, which led to lower levels of Nrf2 target genes such as haem oxygenase\u20101 (HO\u20101) and NAD(P)H quinone dehydrogenase 1 (NQO1). Furthermore, OTA disturbed the equilibrium between apoptosis and survival, as shown by increased PARP cleavage and cleaved caspase\u20103, as well as decreased Bcl\u20102 expression. In contrast, ISL treatment in OTA\u2010treated mice significantly reduced the liver enzymes, decreased oxidative stress, and restored PI3K\/AKT\/Nrf2 signalling. ISL also increased Nrf2, HO\u20101, NQO1, and Bcl\u20102 while reducing PARP cleavage and cleaved caspase\u20103. These findings indicate that ISL mitigates OTA\u2010induced liver damage by activating the Nrf2 signaling pathway, thereby reducing oxidative stress and cellular apoptosis.<\/jats:p>","DOI":"10.1002\/jbt.70408","type":"journal-article","created":{"date-parts":[[2025,7,24]],"date-time":"2025-07-24T07:20:03Z","timestamp":1753341603000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Isoliquiritigenin Attenuates Ochratoxin A\u2010Induced Hepatic Oxidative Stress and Toxicity Through the PI3K\/AKT\/Nrf2 Pathway in Swiss Albino Mice"],"prefix":"10.1002","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8048-7378","authenticated-orcid":false,"given":"Mayyadah Abdullah","family":"Alkuwayti","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, College of Science King Faisal University Al\u2010Ahsa Saudi 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