Indian Journal of Animal Research
SCOPUSWeb of Science
  • Year: 2026
  • Volume: 60
  • Issue: 9

Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

  • Author:
  • Hebah Alabbad1, Manal Alfwuaires1, Ashraf M. Abdel-Moneim2, Hany Elsawy3,4,*, Nourah Almulhim3, Ademola C. Famurewa5,6, Azza Sedky1,2
  • Total Page Count: 6
  • Page Number: 1612 to 1617

1Department of Biological Sciences, College of Science, King Faisal University, Al-Ahsa, 31982, Saudi Arabia

2Department of Zoology, Faculty of Science, Alexandria University, Alexandria, Egypt

3Department of Chemistry, College of Science, King Faisal University, PO Box 400Al-Ahsa, 31982, Saudi Arabia

4Department of Chemistry, Faculty of Science, Tanta University, Tanta, Egypt

5Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria

6Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal-576 104, Karnataka, India

*Corresponding Author: Hany Elsawy, Department of Chemistry, College of Science, King Faisal University, PO Box 400 Al-Ahsa, 31982, Saudi Arabia, Email: hmostafa@kfu.edu.sa

Abstract

Carbon tetrachloride (CCl4) is a critical hepatotoxicant causing liver injury and fibrosis via hepatic production of reactive oxygen species (ROS). Apigenin (APG) is a natural bioactive compound and flavonoid antioxidant. We, therefore, evaluated whether APG could mitigate CCl4-mediated hepatotoxicity.

Rats were randomly divided and administered APG and/or CCl4 in Control group, CCl4 group, APG + CCl4 groups (APG: 10 and 20 mg/kg bw) and APG groups (APG: 10 and 20 mg/kg bw) 2 times per week for 7 consecutive weeks.

Rats exposed to CCl4 demonstrated marked increases in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and monoamine oxidase (MAO) activities and decreased hepatic malondialdehyde (MDA) level compared to control. The hepatic activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) decreased appreciably. The CCl4 intoxication caused significant increases in inflammatory cytokines (IL-6 and TNF-α) and apoptosis markers, while the anti inflammatory cytokines (IL-4 and IL-10) decreased with evident histopathological lesions compared to control. APG-dose-dependently prevented these hepatic alterations.

Keywords

Apigenin, Carbon tetrachloride, Hepatotoxicity