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

Autor: Tabaa MME; Pharmacology & Environmental Toxicology, Environmental Studies & Research Institute (ESRI), University of Sadat City, Minofia Governorate, Sadat city, Egypt. manar.eltabaa@esri.usc.edu.eg., Aboalazm HM; Biochemistry, Environmental Studies & Research Institute (ESRI), University of Sadat City, Sadat City, Egypt., Shaalan M; Pathology Department, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt., Khedr NF; Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, Egypt.
Jazyk: angličtina
Zdroj: Inflammopharmacology [Inflammopharmacology] 2022 Jun; Vol. 30 (3), pp. 961-980. Date of Electronic Publication: 2022 Apr 02.
DOI: 10.1007/s10787-022-00961-9
Abstrakt: 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.
(© 2022. The Author(s).)
Databáze: MEDLINE
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