Silymarin constrains diacetyl-prompted oxidative stress and neuroinflammation in rats: involvements of Dyn/GDNF and MAPK signaling pathway

Neuroinflammation, a major component of many CNS disorders, has been suggested to be associated with diacetyl (DA) exposure. DA is commonly used as a food flavoring additive and condiment. Lately, silymarin (Sily) has shown protective and therapeutic effects on neuronal inflammation. The study aimed...

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Bibliographic Details
Published in:Inflammopharmacology 2022-06, Vol.30 (3), p.961-980
Main Authors: Tabaa, Manar Mohammed El, Aboalazm, Hamdi M., Shaalan, Mohamed, Khedr, Naglaa Fathy
Format: Article
Language:English
Subjects:
Allergology
Animals
Biomedical and Life Sciences
Biomedicine
Dermatology
Diacetyl
Gastroenterology
Glial Cell Line-Derived Neurotrophic Factor
Immunology
Neuroinflammatory Diseases
Original
Original Article
Oxidative Stress
Pharmacology/Toxicology
Rats
Rheumatology
Signal Transduction - physiology
Silymarin - pharmacology
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Summary:Neuroinflammation, a major component of many CNS disorders, has been suggested to be associated with diacetyl (DA) exposure. DA is commonly used as a food flavoring additive and condiment. Lately, silymarin (Sily) has shown protective and therapeutic effects on neuronal inflammation. The study aimed to explore the role of Sily in protecting and/or treating DA-induced neuroinflammation. Neuroinflammation was induced in rats by administering DA (25 mg/kg) orally. Results revealed that Sily (50 mg/kg) obviously maintained cognitive and behavioral functions, alleviated brain antioxidant status, and inhibited microglial activation. Sily enhanced IL-10, GDNF and Dyn levels, reduced IFN-γ, TNFα, and IL-1β levels, and down-regulated the MAPK pathway. Immunohistochemical investigation of EGFR and GFAP declared that Sily could conserve neurons from inflammatory damage. However, with continuing DA exposure during Sily treatment, oxidative stress and neuroinflammation were less mitigated. These findings point to a novel mechanism involving the Dyn/GDNF and MAPK pathway through which Sily might prevent and treat DA-induced neuroinflammation.
ISSN:0925-4692
1568-5608
DOI:10.1007/s10787-022-00961-9