Journal
PHARMACEUTICALS
Volume 15, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/ph15121563
Keywords
piracetam; chemobrain; doxorubicin; acetylcholinesterase; neuroinflammation; apoptosis; oxidative stress
Categories
Funding
- Deanship of Scientific Research, Qassim University, Saudi Arabia [10223-pharmacy-2020-1-3-I]
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This study found that piracetam (PIRA) can significantly reduce doxorubicin (DOX)-induced cognitive deficits in a rat model. It achieves this by reducing acetylcholinesterase (AChE) levels, suppressing neuroinflammatory mediators, decreasing pro-apoptotic proteins, and reducing oxidative stress.
Cancer chemotherapy is known to cause cognitive defects in patients. Our study investigated the effect of piracetam (PIRA; 200 or 400 mg/kg) against doxorubicin (DOX)-induced cognitive deficits in a rat model. The cognitive parameters were analyzed using elevated plus-maze, novel object recognition, and Y-maze tests. Acetylcholinesterase (AChE), neuroinflammatory mediators (cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), nuclear factor-kappa B (NF-kappa B), tumor necrosis factor-alpha (TNF-alpha)), apoptotic proteins (B-cell lymphoma-2 (Bcl-2), Bcl2 associated X protein (Bax), cysteine aspartate specific protease-3 (caspase-3)), oxidative parameters (malondialdehyde (MDA), catalase (CAT), and glutathione (GSH)) were also determined in the brain. PIRA administration offered significant protection against DOX-induced cognitive deficits in all maze tests and restored cholinergic functions via a significant reduction in AChE levels. Additionally, PIRA suppressed DOX-induced neuroinflammatory mediators (COX-2, PGE2, NF-kappa B, and TNF-alpha), pro-apoptotic proteins (Bax and caspase-3), and oxidative stress (MDA). Besides, it facilitated antioxidant (CAT and GSH) levels. Hence, our study highlighted that the neuroprotective activity of PIRA against DOX-induced cognitive deficits can be linked to reductions of AChE levels, neuro-inflammatory mediators, pro-apoptotic proteins, and oxidative stress.
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