Lycopene ameliorates propionic acid‐induced autism spectrum disorders by inhibiting inflammation and oxidative stress in rats

Erten, Füsun

doi:10.1111/jfbc.13922

Cited by 14 publications

(4 citation statements)

References 69 publications

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“…This confirmed both the implication that IFN-γ was involved in stimulating the release of ROS from microglia in PPA-treated rats and the efficacy of bee pollen as an antioxidant and anti-inflammatory product, through the remarkable correction of both signaling related variables [41]. This is supported by the recent work of Erten [44] in which attenuation of postnatal PPA-induced oxidative stress and neuroinflammation in rats was treatable and accompanied an improvement in the autism-like behavioral phenotypes induced.…”

Section: Discussionsupporting

confidence: 75%

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

et al. 2022

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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).

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Section: Discussionsupporting

confidence: 75%

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

et al. 2022

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“…The results are matched with [27] . ID has also been linked to malfunctioning of the brain's cholinergic system [22] which resulted in low levels of ACh as a potential contributor to ID symptomatology. Inflammation, cell apoptosis, and increased oxidative stress are observed during neurodegenerative diseases and depressive disorders [50] .…”

Section: Discussionmentioning

confidence: 99%

Reciprocal crosslink among MeCP2/BDNF /CREB signaling pinpointed in autism spectrum disorder

Mahmoud,

Elhefnawei,

EL-Desouky

et al. 2024

Toxicology Reports

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“…Oxidative stress is one of the multiple mechanisms involved in PRA-induced liver toxicity [19]. Moreover, a recent study by Erten has reported that PRA increases ROS generation mediated by polyunsaturated fatty acid oxidation and produces MDA, which is responsible for biomolecular organ damage [20]. In the current study, both A-CAR and L-CoQ 10 significantly attenuated PRA-induced oxidative stress by improving the activity of the SOD enzyme and the levels of endogenous GSH and reducing MDA levels.…”

Section: Discussionmentioning

confidence: 99%

Acetyl-L-Carnitine and Liposomal Co-Enzyme Q10 Attenuate Hepatic Inflammation, Apoptosis, and Fibrosis Induced by Propionic Acid

Alhusaini

Alsoghayer

Alhushan

et al. 2023

IJMS

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Propionic acid (PRA) is a metabolic end-product of enteric bacteria in the gut, and it is commonly used as a food preservative. Despite the necessity of PRA for immunity in the body, excessive exposure to this product may result in disruptive effects. The purpose of this study is to examine the hepatoprotective effects of acetyl-L-carnitine (A-CAR) and liposomal-coenzyme Q10 (L-CoQ10) against PRA-induced injury. Liver injury in rats was induced by oral administration of PRA, and A-CAR and L-CoQ10 were administered concurrently with PRA for 5 days. Oxidative stress, inflammatory, apoptotic, and fibrotic biomarkers were analyzed; the histology of liver tissue was assessed as well to further explore any pathological alterations. PRA caused significant increases in the levels of serum liver enzymes and hepatic oxidative stress, inflammatory, and apoptotic biomarker levels, along with histopathological alterations. Concurrent treatment with A-CAR and/or L-CoQ10 with PRA prevented tissue injury and decreased the levels of oxidative stress, proinflammatory cytokines, and apoptotic markers. Additionally, A-CAR and/or L-CoQ10 modulated the expression of high-mobility group box-1, cytokeratin-18, transforming growth factor-beta1, and SMAD3 in liver tissue. In conclusion, A-CAR and/or L-CoQ10 showed hepatoprotective efficacy by reducing oxidative stress, the inflammatory response, apoptosis, and fibrosis in liver tissue.

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Lycopene ameliorates propionic acid‐induced autism spectrum disorders by inhibiting inflammation and oxidative stress in rats

Cited by 14 publications

References 69 publications

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

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

Reciprocal crosslink among MeCP2/BDNF /CREB signaling pinpointed in autism spectrum disorder

Acetyl-L-Carnitine and Liposomal Co-Enzyme Q10 Attenuate Hepatic Inflammation, Apoptosis, and Fibrosis Induced by Propionic Acid

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