ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Comparative hepatoprotective effects of Ginkgo biloba extract and N-Acetylcysteine against methotrexate-induced liver injury in rats: modulation of IκB-α, p38 MAPK, and p53 phosphorylation.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Methotrexate (MTX) is an effective chemotherapeutic agent whose use can be limited by hepatotoxicity. This study comparatively evaluated the effects of Ginkgo biloba extract (GbE) and N-acetylcysteine (NAC) on MTX-induced liver injury, focusing on oxidative stress, inflammatory and apoptotic responses, and associated hepatic phosphorylation of Inhibitor of nuclear factor kappa-B alpha (IκB-α), p38 mitogen-activated protein kinase (p38 MAPK), and tumor protein p53 (p53), key components of stress-responsive signaling pathways. Thirty-two adult male rats were randomly assigned to four groups (n = 8/group). MTX (20 mg/kg, i.p.) was administered once on Day 4. GbE or NAC (200 mg/kg, p.o.) was administered for 3 days before and 6 days after MTX exposure. Serum alanine aminotransferase (ALT), total and direct bilirubin and hepatic malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), tumor necrosis factor- alpha (TNF-α), interleukin-1 beta (IL-1β), Bcl-2-associated X protein (Bax), and B-cell lymphoma 2 (Bcl-2) were assessed. Hepatic phosphorylation of IκBα, p38 MAPK, and p53 was evaluated by Western blotting. MTX significantly (P < 0.001) increased serum ALT by 120% and hepatic MDA, TNF-α, IL-1β and Bax by 127%, 386%, 163%, and 439%, respectively, while reducing GSH and Bcl-2 by 66% and 63%, relative to control. Phosphorylation of IκBα, p38 MAPK, and p53 increased by 35%, 64%, and 68%, respectively. GbE and NAC significantly (P < 0.001) attenuated these alterations, with NAC producing generally greater effects than GbE. GbE and NAC attenuated MTX-induced hepatic injury across interconnected oxidative, inflammatory, apoptotic, and signaling endpoints. NAC showed a generally stronger response under the conditions tested. These findings support further investigation of both agents as potential strategies for mitigating MTX-associated hepatotoxicity.
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