Luteolin Alleviates AflatoxinB1-Induced Apoptosis and Oxidative Stress in the Liver of Mice through Activation of Nrf2 Signaling Pathway
| Autor: | Attalla F. El-kott, Aftab Shaukat, Dost Muhammad Baloch, Rana Waseem Akhtar, Papliński Rafał, Mohamed M. Abdel-Daim, Imran Rashid Rajput, Kuntan Wu, Shahid Ali Rajput, Agnieszka Najda, Ashraf Albrakati, Muhammad Asif Raza |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Nrf2 signaling pathway
Aflatoxin Antioxidant Physiology medicine.medical_treatment Clinical Biochemistry SOD1 RM1-950 Pharmacology medicine.disease_cause Biochemistry chemistry.chemical_compound medicine oxidative stress luteolin Molecular Biology Liver injury Chemistry apoptosis Cell Biology medicine.disease GCLC Apoptosis aflatoxin B1 Therapeutics. Pharmacology Luteolin Oxidative stress liver injury |
| Zdroj: | Antioxidants Volume 10 Issue 8 Antioxidants, Vol 10, Iss 1268, p 1268 (2021) |
| ISSN: | 2076-3921 |
| DOI: | 10.3390/antiox10081268 |
| Popis: | 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 (n = 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. |
| Databáze: | OpenAIRE |
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