Naringenin's Neuroprotective Effect on Diazino-Induced Cerebellar Damage in Male Albino Rats, with Modulation of Acetylcholinesterase.

Abstract

Background: Diazinon, a well-known organophosphorus compound, is recognized for its neurotoxic effects, primarily through the inhibition of acetylcholinesterase (AChE) and induction of oxidative stress.

Aim: This study evaluates the neuroprotective effects of naringenin, a citrus flavonoid, against diazinon-induced cerebellar damage in male albino rats.

Materials and methods: Twenty-four rats were divided into four groups: control, naringenin, diazinon, and diazinon with naringenin.

Results: Histological examination revealed altered structures of Purkinje cells in the cerebellum of the diazinon group. Naringenin co-treatment significantly improved cerebellar histology and modulated oxidative stress markers by decreasing malondialdehyde (MDA) and increasing glutathione (GSH) and glutathione peroxidase (GPx) levels. Additionally, naringenin exhibited anti-inflammatory effects by decreasing nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) levels, while increasing interleukin-10 (IL-10). It also reduced apoptotic markers, including p53, Bax, caspase-9, caspase-8, and caspase-3, while increasing the anti-apoptotic marker Bcl-2. Furthermore, naringenin modulated AChE activity, leading to decreased acetylcholine levels and reduced neurotoxicity.

Conclusions: These findings suggest that naringenin's antioxidant, anti-inflammatory, and anti-apoptotic properties contribute to its neuroprotective role against diazinon-induced cerebellar damage.