Apigenin alleviated acetaminophen‐induced hepatotoxicity in low protein‐fed rats: Targeting oxidative stress, STAT3, and apoptosis signals. Issue 5 (11th February 2020)

• Record Type: Journal Article
• Authors: Mohamed, Wafaa R.; Kotb, Amr S.; Abd El‐Raouf, Ola M.; Mohammad Fikry, Ebtehal
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 34:Issue 5(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-02-11
• Subjects: acetaminophen -- apigenin -- apoptosis -- hepatotoxicity -- protein malnutrition; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22472
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: Apigenin (API) is a natural flavonoid abundant in fruits and vegetables. The present study was undertaken to evaluate the effect of protein malnutrition (PMN) on acetaminophen (APAP)‐induced hepatotoxicity, together with the protective effects of API, in male Wistar albino rats. In total, 64 male rats were divided into eight groups. Silymarin (SIL) (100 mg/kg, PO) as a reference standard and API (50 mg/kg, PO) were given to normal and APAP‐induced hepatic injury in low protein‐fed rats. The present results revealed that PMN significantly potentiated APAP‐induced hepatotoxicity. Interestingly, the administration of SIL and API alleviated the induced damage, as revealed by reduced serum alanine aminotransferase and aspartate aminotransferase activities along with a significant improvement of the histopathological damage. API suppressed inflammatory response by reducing the interleukin‐1β level and signal transducer and activator of transcription 3 expressions along with attenuating oxidative stress as shown by a significant reduction in liver contents of malondialdehyde and nitrite/nitrate as well as restoration of hepatic content of reduced glutathione and superoxide dismutase activity. API also counteracted apoptosis through downregulation of caspase‐3 expression level. In conclusion, PMN greatly potentiated the hepatotoxic effects of APAP, and API produced a multimechanistic hepatoprotective activity that can be attributed to its antioxidant, anti‐inflammatory, and antiapoptotic effects.