Luteolin Alleviates AflatoxinB₁-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway

• Main Authors: Shahid Ali Rajput (Author), Aftab Shaukat (Author), Kuntan Wu (Author), Imran Rashid Rajput (Author), Dost Muhammad Baloch (Author), Rana Waseem Akhtar (Author), Muhammad Asif Raza (Author), Agnieszka Najda (Author), Papliński Rafał (Author), Ashraf Albrakati (Author), Attalla F. El-Kott (Author), Mohamed M. Abdel-Daim (Author)
• Format: Book
• Published: MDPI AG, 2021-08-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

Aflatoxin B₁ (AFB₁), a threatening mycotoxin, usually provokes oxidative stress and causes hepatotoxicity in animals and humans. Luteolin (LUTN), well-known as an active phytochemical agent, acts as a strong antioxidant. This research was designed to investigate whether LUTN exerts protective effects against AFB₁-induced hepatotoxicity and explore the possible molecular mechanism in mice. A total of forty-eight mice were randomly allocated following four treatment groups (<i>n</i> = 12): Group 1, physiological saline (CON). Group 2, treated with 0.75 mg/kg BW aflatoxin B₁ (AFB₁). Group 3, treated with 50 mg/kg BW luteolin (LUTN), and Group 4, treated with 0.75 mg/kg BW aflatoxin B₁ + 50 mg/kg BW luteolin (AFB₁ + LUTN). Our findings revealed that LUTN treatment significantly alleviated growth retardation and rescued liver injury by relieving the pathological and serum biochemical alterations (ALT, AST, ALP, and GGT) under AFB₁ exposure. LUTN ameliorated AFB₁-induced oxidative stress by scavenging ROS and MDA accumulation and boosting the capacity of the antioxidant enzyme (CAT, T-SOD, GSH-Px and T-AOC). Moreover, LUTN treatment considerably attenuates the AFB₁-induced apoptosis in mouse liver, as demonstrated by declined apoptotic cells percentage, decreased Bax, Cyt-c, caspase-3 and caspase-9 transcription and protein with increased Bcl-2 expression. Notably, administration of LUTN up-regulated the Nrf2 and its associated downstream molecules (HO-1, NQO1, GCLC, SOD1) at mRNA and protein levels under AFB₁ exposure. Our results indicated that LUTN effectively alleviated AFB₁-induced liver injury, and the underlying mechanisms were associated with the activation of the Nrf2 signaling pathway. Taken together, LUTN may serve as a potential mitigator against AFB₁-induced liver injury and could be helpful for the development of novel treatment to combat liver diseases in humans and/or animals.

Item Description

10.3390/antiox10081268
2076-3921