氧化应激
神经炎症
胶质细胞源性神经生长因子
MAPK/ERK通路
化学
信号转导
药理学
双乙酰
医学
炎症
免疫学
生物化学
受体
神经营养因子
作者
Manar Mohammed El Tabaa,Hamdi M Aboalazm,Mohamed Shaalan,Naglaa F. Khedr
标识
DOI:10.1007/s10787-022-00961-9
摘要
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.
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