Ameliorative effect of bee venom and its extracted bradykinin-potentiating factor on neurological alteration induced by acrylamide and chips administration

Abstract

BackgroundAcrylamide is reported for its toxicity on the central and the peripheral nervous system and causes paralysis. Bee venom (BV) and bradykinin-potentiating factor (BPF) have been documented for their potential therapeutic effects as anti-neuroinflammation. The study aimed to ameliorate the neurotoxic effects of acrylamide or chips by using BV or its extracted BPF. Mice were divided into 15 subgroups: control (G1.1, G1.2, G1.3) at 30, 45, and 60 days, respectively; acrylamide- (10 mg/kg b.w.; orally daily) administered subgroup for 30 days (G2.1), 45 days (G2.2), and 60 days (G2.3); chips feeding group (1/3 of daily diet) for 30 days (G3.1), 45 days (G3.2), and 60 days (G3.3); bee venom-treated group for 60 days (1.319 mg/kg b.w.) (G4.1); BPF-treated group for 60 days (2.314 mg/kg b.w.) (G4.2), day after the other day; and acrylamide- or chips-administered groups combined either with BV (G5.1, G6.1) or BPF treatment (G5.2, G6.2) for 60 days.ResultsThe results indicated that the approximate LD50 for BV and BPF equal to 13.19 mg/kg and 23.14 mg/kg, respectively, and the extracted BPF contains 15 amino acids. Also, the results showed abnormal gait in mice of acrylamide-administered groups which was accompanied by histopathological changes in the hippocampus, cerebellum, and cerebral cortex. A marked gradual increase of alpha-synuclein expression was noted at the studied region in the acrylamide- and chips-treated groups at 60 days of treatment as compared to control. Both BV- and BPF-treated groups either separately or in co-administration with acrylamide or with chips did not show any histopathological changes in the studied regions with downregulated expression of alpha-synuclein.ConclusionThe study concluded the neuroprotective effect of BV and its extracted BPF against neurotoxicity induced by acrylamide or chips administration.