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Neuroprotective efficacy of nano‐CoQ against propionic acid toxicity in rats: Role of BDNF and CREB protein expressions
Author(s) -
Alhusaini Ahlam,
Hasan Iman H.,
Alrumayyan Bashayer,
Alesikri Marwa,
Alanazi Khansa,
Almasoud Rawan,
Almarshad Sarah
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22449
Subject(s) - creb , neuroprotection , neurotoxicity , pharmacology , neurotrophic factors , chemistry , glutathione , superoxide dismutase , brain derived neurotrophic factor , carnitine , toxicity , antioxidant , endocrinology , biochemistry , medicine , receptor , transcription factor , gene , enzyme
Propionic acid (PRA) is used as a food preservative. This study was aimed to investigate the neuroprotective effect of acetyl‐ l ‐carnitine (ALC) and nano‐Coenzyme Q (N‐CoQ) on brain intoxication induced by PRA in rats. Rats were divided into five groups: group I: control; group II: received PRA; group III: received ALC; group IV: received N‐CoQ; and group V: received ALC and N‐CoQ for 5 days. The antioxidants in question markedly ameliorated serum interleukin‐1β and tumor necrosis factor‐α, and brain NO, lipid peroxide, glutathione, and superoxide dismutase levels as well as protein expression of brain‐derived neurotrophic factor (BDNF) and P‐cyclic‐AMP response element‐binding protein (CREB) that were altered by a toxic dose of PRA, as well as histopathological alterations, including improvement of the cerebellum architecture. Interestingly, the combination therapy of ALC and N‐CoQ achieved the most neuroprotective effect compared with monotherapies. The current study established that N‐CoQ is considered as a useful tool to prevent brain injury induced by PRA. BDNF and CREB proteins are involved in both PRA neurotoxicity and treatment.