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ORIGINAL RESEARCH article

Front. Mol. Biosci.
Sec. Cellular Biochemistry
Volume 11 - 2024 | doi: 10.3389/fmolb.2024.1507786

Avenanthramide-C ameliorate doxorubicin-induced hepatotoxicity via modulating Akt/GSK-3β and Wnt-4/β-Catenin pathways in male rats

Provisionally accepted
Maha A. Alwaili Maha A. Alwaili 1Salwa Aljohani Salwa Aljohani 2Amal Abu-Almakarem Amal Abu-Almakarem 3Sahar A. Alkhodair Sahar A. Alkhodair 4Maha Al-Bazi Maha Al-Bazi 4Thamir Eid Thamir Eid 4Maysa Mobasher Maysa Mobasher 5Norah K Algarzae Norah K Algarzae 6Arwa I. Khayyat Arwa I. Khayyat 6Luluah alshaygy Luluah alshaygy 6Karim S. El-Said Karim S. El-Said 7,8*
  • 1 Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia
  • 2 College of Science, Taibah University, Yanbu, Saudi Arabia
  • 3 Department of Basic Sciences, Faculty of Applied Medical Sciences, Al-Baha University, Al-Baha, Saudi Arabia
  • 4 King Abdulaziz University, Jeddah, Makkah, Saudi Arabia
  • 5 College of Medicine, Jouf University, Sakakah, Saudi Arabia
  • 6 King Saud University, Riyadh, Riyadh, Saudi Arabia
  • 7 Tanta University, Tanta, Egypt
  • 8 Faculty of Science, Tanta University, Tanta, Gharbia, Egypt

The final, formatted version of the article will be published soon.

    Background: Doxorubicin (DOX) drugs for used in cancer treatment can cause various adverse effects, including hepatotoxicity. Natural-derived constituents showed have shown promising ameliorative effects againsteffects in alleviating chemotherapy-induced toxicities.This study addressed the effect of Avenanthramides-C (AVN-C) treatment in rats with DOXindued hepatotoxicity.Methods: AutoDock Vina was used for the molecular docking investigations. In silico toxicity prediction for AVN-C and DOX was performed using the Pro Tox-III server. Four groups of ten male Sprague-Dawley rats were created as follows: Group 1 (Gp1) served as a negative control, Gp2 received an intraperitoneal (i.p.) injection of AVN-C (10 mg/kg), Gp3 received an intraperitoneal (i.p.) dose of DOX (4 mg/kg) each weekly for a month, and Gp4 received the same dose of DOX as G3 and AVN-C as G2. Histopathological, molecular, and biochemical analyses were assessed conducted one month later.The results demonstratedstudy showed that treatment with AVN-C showed a significantly ameliorated ive efficacy against DOX-induced hepatotoxicity in rats by restoring the biochemical alterations, boosting antioxidant activity, mitigating reducing inflammation, and modulating the Akt/GSK-3β and Wnt-4/β-Catenin signaling pathways in male rats.The This study is the first to demonstrate the therapeutic effects of AVN-C therapy on DOX-induced liver damage in male rats were addressed for the first time in this study. Therefore, AVN-C could have a pronounced palliative effect on the hepatotoxicity induced caused by DOX treatment. These findings suggest that AVN-C could potentially alleviate the hepatotoxicity adverse effect of DOX duringassociated with DOX-based chemotherapy.

    Keywords: Font: 12 pt, Complex Script Font: 12 pt, Not Superscript/ Subscript Avenanthramides, Antioxidants, anti-inflammatory, Doxorubicin, Hepatotoxicity, signaling pathway

    Received: 08 Oct 2024; Accepted: 06 Nov 2024.

    Copyright: © 2024 Alwaili, Aljohani, Abu-Almakarem, Alkhodair, Al-Bazi, Eid, Mobasher, K Algarzae, Khayyat, alshaygy and El-Said. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Karim S. El-Said, Tanta University, Tanta, Egypt

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.