Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway

The current study aimed to investigate the potential protective role of boswellic acids (BAs) against doxorubicin- (DOX-) induced hepatotoxicity. Also, the possible mechanisms underlying this protection; antioxidant, as well as the modulatory effect on the Nrf2 transcription factor/hem oxygenase-1 (...

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Bibliographic Details
Published in:Oxidative medicine and cellular longevity 2018-01, Vol.2018 (2018), p.1-10
Main Authors: Elbahaie, Alaaeldeen M., Bahr, Hoda I., Ahmed, Hebatalla I., Barakat, Bassant M.
Format: Article
Language:English
Subjects:
Anthracyclines
Antioxidants
Cancer therapies
Deoxyribonucleic acid
DNA
Enzymes
Experiments
Hypotheses
Laboratory animals
Liver
Medical research
Metabolism
Oxidative stress
Pharmacy
Physiology
Rodents
Veterinary medicine
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Summary:The current study aimed to investigate the potential protective role of boswellic acids (BAs) against doxorubicin- (DOX-) induced hepatotoxicity. Also, the possible mechanisms underlying this protection; antioxidant, as well as the modulatory effect on the Nrf2 transcription factor/hem oxygenase-1 (Nrf2/HO-1) pathway in liver tissues, was investigated. Animals were allocated to five groups: group 1: the saline control, group 2: the DOX group, animals received DOX (6 mg/kg, i.p.) weekly for a period of three weeks, and groups 3–5: animals received DOX (6 mg/kg, i.p.) weekly and received protective doses of BAs (125, 250, and 500 mg/kg/day). Treatment with BAs significantly improved the altered liver enzyme activities and oxidative stress markers. This was coupled with significant improvement in liver histopathological features. BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult. The present results demonstrated that BAs appear to scavenge ROS and inhibit lipid peroxidation and DNA damage of DOX-induced hepatotoxicity. The antioxidant efficacy of BAs might arise from its modulation of the Nrf2/HO-1 pathway and thereby protected liver from DOX-induced oxidative injury.
ISSN:1942-0900
1942-0994
DOI:10.1155/2018/8296451