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. 2022 Jun 21;12(7):571.
doi: 10.3390/metabo12070571.

Protective Effects of Bee Pollen on Multiple Propionic Acid-Induced Biochemical Autistic Features in a Rat Model

Affiliations

Protective Effects of Bee Pollen on Multiple Propionic Acid-Induced Biochemical Autistic Features in a Rat Model

Hanan A Alfawaz et al. Metabolites. .

Abstract

Autism spectrum disorders (ASDs) are neurodevelopmental disorders that clinically presented as impaired social interaction, repetitive behaviors, and weakened communication. The use of bee pollen as a supplement rich in amino acids amino acids, vitamins, lipids, and countless bioactive substances may lead to the relief of oxidative stress, neuroinflammation, glutamate excitotoxicity, and impaired neurochemistry as etiological mechanisms autism. Thirty young male Western albino rats were randomly divided as: Group I-control; Group II, in which autism was induced by the oral administration of 250 mg propionic acid/kg body weight/day for three days followed by orally administered saline until the end of experiment and Group III, the bee pollen-treated group, in which the rats were treated with 250 mg/kg body weight of bee pollen for four weeks before autism was induced as described for Group II. Markers related to oxidative stress, apoptosis, inflammation, glutamate excitotoxicity, and neurochemistry were measured in the brain tissue. Our results indicated that while glutathione serotonin, dopamine, gamma-aminobutyric acid (GABA), GABA/Glutamate ratio, and vitamin C were significantly reduced in propionic acid-treated group (p < 0.05), glutamate, IFN-γ, IL-1A, IL-6, caspase-3, and lipid peroxide levels were significantly elevated (p < 0.05). Bee pollen supplementation demonstrates protective potency presented as amelioration of most of the measured variables with significance range between (p < 0.05)−(p < 0.001).

Keywords: apoptosis; autism spectrum disorders; cytokines; gut microbiota; neurotransmitters; oxidative stress; propionic acid.

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Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Levels of the biomarkers used in ASD (Group II; APP-treated), ASD/bee pollen-protected (Group III), and control (group I) rats. * denotes a statistically significant difference between groups I and II, # denotes a statistically significant difference between groups I and III, and $ denotes statistically significant difference between groups II and III. NE: norepinephrine, 5-HT: serotonin, DA: dopamine, GABA: gamma-aminobutyric acid, Glut: glutamate, Gln: glutamine, IFN-γ: interferon gamma, IL-x: interleukin x, VEGF: vascular endothelial growth factor, TNF-α: tumor necrosis factor alpha, Casp-3: caspase 3, GSH: glutathione, VitC: vitamin C, LipPerox: lipid peroxidase.
Figure 2
Figure 2
Average Bacterial counts in fecal samples of control, PPA-induced rodent model of autism, and bee pollen-protected autism model. NA: nutrient agar, MAC: MacConkey’s agar, BA: blood agar, CCFA: cycloserine cefoxitin fructose agar, BBE: Bacteroides bile esculin agar. Nutrient agar—Gram-positive/Gram-negative rods and cocci; MacConkey—Enterobacteriaceae (Gram-negative rods, lactose fermenters); Blood agar—Gram-positive/Gram-negative rods and cocci; CCFA (Cycloserine Cefoxitin Fructose Agar)—Clostridioides difficile; BBE (Bile Esculin Agar)—Bacteroidetes, streptococci, and enterococci.

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