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Targeting key regulators of hepatic lipid metabolism represents an important therapeutic strategy. Vinpocetine, a phosphodiesterase\u20101 inhibitor, exhibits metabolic and anti\u2010inflammatory properties, but its role in hepatic lipid homeostasis remains insufficiently defined. To evaluate the effect of vinpocetine on hepatic steatosis and its regulatory impact on key lipid\u2010metabolism genes, including peroxisome proliferator\u2010activated receptor\u2010\u03b1 (PPAR\u2010\u03b1), PPAR\u2010\u03b3, sterol regulatory element\u2010binding protein\u20101c (SREBP\u20101c), and fatty acid translocase\/cluster of differentiation 36 (FAT\/CD36), in an experimental NAFLD model. NAFLD was induced in rats using a high\u2010fat diet. Animals received vinpocetine (10\u2009mg\/kg, i.p.) daily for 5 weeks. Hepatic lipid accumulation was assessed histologically and biochemically, while gene expression of PPAR\u2010\u03b1, PPAR\u2010\u03b3, SREBP\u20101c, and FAT\/CD36 was analyzed using RT\u2010PCR. Vinpocetine significantly reduced hepatic lipid accumulation compared with untreated NAFLD controls. It upregulated PPAR\u2010\u03b1 expression while downregulating PPAR\u2010\u03b3, SREBP\u20101c, and FAT\/CD36, indicating enhanced fatty\u2010acid oxidation and reduced lipogenesis and lipid influx. Treatment also improved lipid profile parameters (reduced TC, TG, LDL, and restored HDL), lowered liver enzyme levels, increased antioxidant activity (elevated glutathione), and reduced oxidative and nitrosative stress (decreased malondialdehyde and nitric oxide), accompanied by improved liver histology. Vinpocetine attenuates hepatic steatosis in NAFLD by modulating genes involved in lipid metabolism, suggesting potential therapeutic value. Further studies are required to confirm these findings and clarify mechanisms.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jbt.71005","type":"journal-article","created":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T16:19:49Z","timestamp":1782749989000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Vinpocetine Attenuates Hepatic Steatosis by Modulating Key Lipogenic and Lipid Transport Genes (PPAR\u2010 \u03b3, SREBP, and FAT\/CD36) in Experimental Non\u2010Alcoholic Fatty Liver Disease"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8938-9013","authenticated-orcid":false,"given":"Ekram N.","family":"Abdalhaleem","sequence":"first","affiliation":[{"name":"Department of Clinical Pharmacy and Pharmacology Ibn Sina College for Medical Studies Jeddah Saudi Arabia"},{"name":"Department of Pharmacology and Toxicology, Faculty of Pharmacy Al\u2010Azhar University Cairo Egypt"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7832-4556","authenticated-orcid":false,"given":"Bashir A.","family":"Yousef","sequence":"additional","affiliation":[{"name":"Department of Clinical Pharmacy and Pharmacology Ibn Sina College for Medical Studies Jeddah Saudi Arabia"},{"name":"Department of Pharmacology, Faculty of Pharmacy University of Khartoum Khartoum Sudan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,6,29]]},"reference":[{"key":"e_1_2_10_2_1","unstructured":"N.Chalasani Z.Younossi J. 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