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

Abstract

Background: Acrylamide 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. Results: The 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. Conclusion: The study concluded the neuroprotective effect of BV and its extracted BPF against neurotoxicity induced by acrylamide or chips administration.

Effect of a bradykinin potentiating factor separated from honey bee venom on thyroid gland and testis in hypothyroid white rats

“…This is noticed by injection of BPF in sublethally-irradiated and non-irradiated Guinea pigs (Salman, 2002). Also, bee venom and its bradykinin-potentiating factor are therapeutic agents in the neurodegenerative diseases in which α-synucloin plays the effective role in Parkinson's disease (Lashein et al, 2018). In addition, bradykinin-potentiating peptides are considered a useful tool in developing antihypertensive drugs to expand the range of therapies to control hypertension (Lewis & Garcia, 2003).…”

Bradykinin Potentiating Factor from Egyptian Honey Bee Venom Fraction: A Potential Therapeutic Agent for Type 1 Diabetes

“…injection, following the method described by Meier and Theakston [31]. This method was carried out by our colleagues [20] and involved administering varying doses of BV and BPF to a group of experimental animals and observing the dose at which 50% of the animals showed lethal effects.…”

Bee Venom Activates the Nrf2/HO-1 and TrkB/CREB/BDNF Pathways in Neuronal Cell Responses against Oxidative Stress Induced by Aβ1–42

“…On day 1, except for the naïve group that received 3 µL of PBS, all mice were injected with 3 µL of a solution containing 3 µg of Aβ 1-42 . A bee venom maximum safe dosage of approximately 13.19 mg/kg was previously determined [44]. Another study applied 0.1 mg/kg of bee venom into a mouse vascular neurodegenerative model [45].…”